Bedside Techniques: Methods of Clinical Examination [Fifth (2019) ed.] 9789696375258

Table of contents :
1. History Taking
2. Physical Examination
3. Cardiovascular System
4. Respiratory System
5. Alimentary and Genito-Urinary System
6. Nervous System
7. Pediatric Clinical Examination
8. How To Present A Case?
9. Normal Values
Index

Citation preview

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Bedside · Techniques Methods of Clinical Examination Fifth Edition

BEDSIDE TECHNIQUES Methods of Clinical Examination Fifth Edition A Book for Medical Students and Doctors

By

Muhammad Inayatullah FRCP (London) Professor of Medicine Multan Medical and Dental College Multan

Shabbir Ahmed Nasir FRCPE Principal Multan Medical and Dental College Multan

Paramount Books (Pvt.) Ltd. I

I

I

I

I

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Karachi Lahore Islamabad Hyderabad Faisalabad Peshawar Abbottabad

© Paramount Boo - (

L.) Ltd.

es Bedside ec Methods of Clinica Exa ination by Muhammad lnayatullah S a oir Ahmed Nasir All rights reserved. No part of this publication may be reproooced. stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, pho oco · . recording or otherwise, without the prior permission of the Copyright Holders. This book is sold subject to the condition that it shall no by way o' e or otherwise, be lent, resold, hired out or otherwise circulated without the publisher's prior consent in a y • oinding or cover other than that in which it is published·and without a similar condition including this cond· · being imposed on the subsequent purchaser. Disclaimer: Readers are strongly advised to confirm that the in o a ·on, especially with regard to drug usage, complies with the latest legislation and standards of practice. e p blisher and the author do not assume any responsibility for any loss or injury and/or damage to a person or property arising out of (or related to) any use of the material contained in this book. Furthermore, it is an academic responsibility on the readers' part to inform the Publisher about inaccuracy, misprint or typographical error (if any. Copyright© 2019 All Rights

Reserved

First Edition ................................ 1995 Second Edition .......................... 2001 Third Edition .............................. 2006 Fourth Edition ........................... 2013 Fifth Edition ................................ 2019 Reprint ......................................... 2020 Reprint ......................................... 2021 Reprint .........................................2022 Reprint .........................................2023

Paramount Books (Pvt.) Ltd. 152/0. Block-2. P.E.C.H.S .. Karachi- 7 5400. Tel: +9 2-21-34310030. info®paramountbooks.com.pk www.paramountbooks.com.pk

ISBN: 978-969-637-525-8

111

Dedication Dedicated to Our Teachers

Pref ace to First Edition The que rion most freq uently asked of u ,n why we ever wanted to w rite about cl inical methods ,,·hen there were so m any other books al ready in the market. This is probably the right place to an \\·er this question ... As teachers and examiner in Medicine we had been aware for a long time of the unenviable position of the brilliant medical cudent who has learnt the method of exam ination, the differential diagnosis, the significance of probabilities in their proper order, and the preferred investigation s from fo reign books. only to face the w rath of the examiner w ho is more realistically aware of the different local di sease pre\·alence and diagnostic med ical faci lities. We have b een aware too of the plight of the average medical srudent for w hom English remains a relative ly difficult fo reign language whose nuances are completely lost upon him and who needs to struggle not on ly w ith already difficult concepts of clinical M edicine but also has to decipher (subtle but significant) shades of m eaning w hich are obvious only co the native speaker of the English language; and a problem common to all students - the sequence of narration of information given in books is very different from what is taught and e:x.'])ected of them. When faced w ith these problem s the students resort co "notes" prepared by other students and full of con ceptual and fac tual errors, or booklets which are little better. They learn w ith great diligence all that is contained w ithin, the truth. half-truth and the gross untruth. They can go through life w ithout ever realizing the myths and fallacies they have imbibed. We thought it was time to address this p roblem, prompting us to w rite this book. We have tried to make this book easily readable for our students. We have tried to do away w ith concepts and material not relevant to local conditions and to put things in the proper perspective, keeping in mind the con straints operating here. But we have also tried to retain all m aterial that the aspi ring post-graduate might need. We have included a large number of line drawings to illustrate concepts: what they lack in artistic quali ty we hope they make up in content and clarity, and should m ake learning relatively easier. The initial interview w ith the patient and the results (h istory taking and presentation) is usually a particularly weak skill with our students and we have attempted to address this problem. We already have a publication which list relevant questions to be asked of the patient according to the main presenting feature and a synopsis of differential diagnosis in tabulated forms (Aids to D iagnostic Process) ; this would be an excellent companion book co strengthen w hat we call "The Art of Relevance". There is a section on Pediatrics, not fou nd in many current books. We think this is very timely considering that Pediatric wi ll soon be a separate subject in the final professional MBBS examination. D eparting from the usual fo rmat. we do not have ections on X-rays and ECG interpretation . Students consult these sections infrequently and very se lectively, usually relying on the ward instructions. We have also not included examination of E N T, Eye and Gynecology; examination in these special ties too is u sually learnt from single subject texts. This has helped in cutting the size and price, and improving "portability" of this book. During the w hole process of w riting of this book we have relied on feedback from our students and young resident staff and we shou ld like to contin ue this process so that subsequent editions can be respo nsive of reader preferences. We would appreciate any comment or suggestion that the reader might make. Muhammad Inayatullah MRC P (UK) Shabbir Ahmad N asir FRCPE Multan 1995

V

Preface To Fifth Edition _-\.re ofhistory taking and methods of physical examination don't change frequently but there arc small and significant changes in understanding of symptomatology and various physical signs overtime. cyle of presentation, composing, printing, illustrations and photographs can be modified to improve rhe readability, understanding, interpretation and reproducibility of the contents. T his edition is a new lookbook with significant improvement in all categories ofcontents and printing quality. Authors hope that this new edition of"Bedside Techniques" with incorporation of latest knowledge will be of ITTeac help in learning of clinical skills for current and future medical graduates. Muhammad Inayatullah MRCP (UK) Shabbir Ahmad Nasir FRCPE Multan 2019

Vl

Foreword I have great pleasure in wntmg a foreword for Bedside Techniques: Methods of Clinical Examination. There is n o dearth of books on clinical examination but w hat distinguishes this book is the stress on explaining the relevant ymptoms and the correct m ethods of eliciting physical signs, this is the real justificatio n for this book. Al l the chapters in this book are clearly wTitten without going into unnecessary details and deserve close study by undergraduate students. postgraduate students and m edical practitioners. Two chapters, on cardiology and neurology. deser,e pecial praise. Cardio logy is a difficult subject to grasp but the method of clinical examination has been clearly e>..'})lained by the author . Detailed de cription of important cardiac conditions has been given along with the approach to history and physical examination. It must be remembered, however, that physical signs sho uld be interpreted \vith the help of relevant investigations li ke chest x-ray, ECG and where possible echocardiography. The chapter on clinical neurology deserves special praise fo r its simplicity and the confidence which it gives to the undergraduate student, not only to carryout clinical examination but also to arrive at a diagn osis. The subject of neurology has been traditionally painted as som ething very difficult to grasp and only meant for specialists: this myth h as been broken in this book. The study of clinical neurology requires a basic understanding of anatomy and physiology, m ore so than any oth er specialty of m edicine and these facets have been clearly e>..1>lained in this book. After studying the chapter on ne urology I am sure that both undergraduate and postgrad uate student w ill find that clinical neu rology is not such a bug bear as traditionally described. T he fact of the matter is that this is one specialty which most commonly allows the correct diagnosis to be m ade on the basis of clinical examination alone ... One of my great teachers use to say that the knowledge of neurology di tingui shes between a good physician and a good quack. I should like to remind the student of an old d ictum "clinical m edicine can be only learnt at the bed side and not by books" but it is equally important that books be consulted to really understand m edicine, I hope the student makes full use of the knowledge contained in this book and practices the ro utines as described to arrive at the correct d iagnosis. I strongly recommend this book to anybody who is interested in clinical m edicine. I feel that this is a significant addition and a breakthrough in the study of clinical m ethods w ritten by local authors. I wish and pray fo r the unqualified success of this book. Dr. Abdul Rauf Ahmad (late)

MD; FRCP (EDIN & LOND) ; FCPS (PAK)

Vll

Acknowledgetnents ang a book is arduo us ... it would be almost impossible if eve1y author didn't have a circle of ::::a:..7Josurc to chemicals or radiations? If yes, w hat is their nature and quantity?

Pain ·u

1

Ask the patient to indicate w here exactly he feels the pain. Pain of duodenal ulcer is in the epigastrium , pai n of ische111ic heart disease is across the sternum and no t over the prccordium while pain of reflux esopl,agitis is along the stern um.

C

E timating duration of pain w itho ut actual m easurement i usually inaccurate, but it i at time helpful in making a diagnosis, e.g., pain of angina usually lasts for less than 30 minutes w hi le that of 111yocardial i11Jarctio11 lasts for m ore than 30 minutes. imilarly, pc rsi tent chc t pain is lcs likely to be due to ischemic heart disease.

ROUTINE QUESTIONS ABOUT CARDINAL SYMPTOMS

Sit o

5

l

Fol lowing terms arc common ly used to describe the character of pain. Diffe rent patients can use different terms to describe the same pain. 1.

H eavin ess

2.

Burning

3.

Aching

4.

Stabbing or cutting

6 Throbbing

7.

Dull

in ureteric colic, distension of abdotnen and con tipation in intestinal colic due to intestinal obstruction .

8.

Gripping

Fever

9.

Pri cki ng

It m eans rise in the bod y tempe rature* above

o li cky

upper limit of normal. Average no rmal body temperature is 98.4°F (37°C) , range is 97 - 99°F (36.6 - 37 .2°C). There i a variation of about on e degree Fahrenheit between morning and evening (di urnal variation), being less in the morning.

J.

6. Jolt like

10.

In colic pe ri ods o f sudden severe pain alternate w ith, eithe r pain free intervals (intestinal colic) o r pain oflesser intensity (ureteric colic).

Frequency and Periodicity of Pain Ask the patient about duration of pa in free intervals and whether this 1s increasing or d ecreasing.

Periodicity m eans patient gets bouts of pain

Fever is a common symptom . Ask the fo llowing questions from all the patie nts presenting w ith fever.

Mode of Onset

for few weeks and then becomes completely symptom free w ithout treatment for few weeks. This cycle is repeated again. This occurs in d11ode11al 11/cer.

Fever due to acute infection s (e.g., m alaria, pneumo nia) is of acute onset w hile feve r due to chro nic infections (e.g. , tuberculosis) and malignancies is of gradual onset.

Special Times of Occurrence

Rigors or Chills

Pain of d11ode11al 11/cer m ay wake the patien t after midnight, but it is neve r present at u sual hours of rising. Pain of sinusitis is maximum few hours after ri sing. H eadac he of 111igra ine may occur during m en ses.

These indicate sudden nse 111 the body temperature. Malaria is a common cause but these can occur in any acute in fectio n li ke pneum onia, urinary tract infection.

Aggravating Factors

Fever of acute infections is of high grade w hile feve r of chronic infectio ns is usually of low

Ask the patient if any particular factor aggravates the pain . M ovements worsen the pain of j o int and muscle disease. Pain of angina is precipitated by exertio n. Pain of peptic ulcer may be worse after tea or spicy food. Pleuritic pain is worse on deep breathing and coughing.

Grade of Fever

grade.**

Relieving Factors Pain of angina is relieved by rest and sublingual nitrates. Pain of d11ode11al ulcer is relieved by food and antacids.

Associated Phenomenon D epending upon underlying disease o ther symptoms may be present, like vomiting in abdo minal pain due to cho lecystitis and headache due to m e ningitis, palpitation and sweating in chest pain of i chem ic heart disease, hematur ia

*

Celsius (centigrade) scale is co mmonly used all ove r the world, but we in Pakistan are m ore fa mi liar w ith the Fahrenheit scale. Formula to convert o ne scale intotheotherisCel iu = Fahrenh eit -32 -:- 1.8 ** There is no p recise d efinitio n of grades of fever. Usually fever of more tha n 102°F (39°C) is considered as high grade and feve r of less than 101 °F (38.5°C) is considered as low grade. If temperature rises above 107°F (41.6°C) it is called hyperpyrexia; if it falls below 95°F (35°C) it is called hypoth ermi a.

-

-

.

-

--

-

-

- --·- -

-

--

·-· - -- -

-

--

Differential diagnosis of abdominal pain Peptic ulcer Cholecystitis Pancreati- Renal pain Ureteric colic tis

Intestinal Hepatitis Appendicitis Worm infestation obstruction

Site

epigastrium

right hypochondrium

epigastrium lumbar region

lumbar region

umbilicus, upper right iliac fossa abdome n

Radiatio n

localized

back, right sh oulder

back

localized

grom

localized

C haracter

gnawmg o r aching

colicky

gnawmg o r cutting

dull

colicky

-

Severity

mild to severe moderate to severe

severe

mild to moderate

Periodicity

present

absent

Special time after midnight no ne of occurrence Aggravating factors

empty stomach

Relieving factors

food and antacids

generalized

right hypochondrium

-

-

aching o r colicky

colicky

aching

moderate to mild to severe m oderate

mild to moderate

moderate to severe

mild to moderate

absent

absent

absent

absent

absent

absent

none

no ne

n o ne

no ne

none

non e

none

fatty meal

no ne

movements m ovements no ne

no ne

no ne

none

none

bending forwards

none

none

none

none

absent

n o ne

no ne

w hole abdo men

()

::r-

Associated pheno mena

vomiting, hem atem esis melena

vomiting, fever

vomiting

unnary sympto m s

vomiting, unnary symptoms

vomiting, fever

-

vomiting, ano reXIa, distension nausea, of abdomen, vom iting obstipatio n

1'> ',:j

r-+

.... (1)

......

I

::r:

c;;· r-+

Signs

tenderness in epigastrium

tenderness in right hypochondrium , Murphy's sign is positive

mild tenderness

tenderness in lumbar Ill region , epigastrium , kidney may hypo tension be palpable

kidney may tenderness, be palpable mass in right if there is iliac fossa h ydronephros1s

anem,a

borborygmi jaundice, tender audible hepatomegaly

....0

---
I

Fig. 2.5: C urved nail with no rmal angle

Fig. 2.7: chamroth ·s sign : Finge r held together space seen at point X in A (normal) is absent in B (clubbing)

15

16 •

Fluctuat ions are pre ent at nail base ;

3.

Ulcerativ e colitis

m ethod to elicit these fluctuatio ns is shown in (Fig. 2.8).

4.

Primary biliary cirrho is

Miscella neous 1.

Familial

2.

Pseudoclu bbing (it is seen in hyperpara thyroidism; there is resorption of terminal phalanx wh ich gives impressio n of clubbing)

Splinter hemorrh ages: These are vertical hemorrha gic streaks under the nails and are commonly seen in manual workers (Fig. 2.9). These can also occur in infective endocarditis.

Leucony chia: These are w hite patches in nail

Fig. 2.8: Method of eliciting fluctuation s in clubbing

•

The curvatur e of the nail is increased , both, in transverse and longitudi nal axi , and nail becomes convex. Normal people can have curved nail but angle is normal (Fig. 2.5)

•

M easure the anteropos terior distance at the level of terminal interphala ngeal joint (A) and also at the level of nai l bed (B).BIA ratio is > 1 in clubbing (Fig. 2.4B)

•

•

Finally, due to overall swelling, terminal phalanx becomes bulbous and rese mbles the end of a drumstic k (Fig. 2.6 A & B). Schamrot h's sign is present. (When two fingers arc approxim ated, normally the re is a space between two nails. It is ab ent is

plates often present in normal persons and are also sometime s een in chronic liver disea e and other condition s causing hypoalbu minemia.

Fig. 2.9: Splinter hemorrhages

Half and half nails: Proximal portion of nails is w hite to pink w hile distal portion is red o r brown. These are seen in chronic renal failure . Pitting of nails: There are a large number of sm all pits in the nails (Fig. 2.10). This occurs in psonas1s.

clubbing; Fig. 2.7).

Causes of Clubbin g Respirat ory disease 1.

Chronic suppurative condition s (bronchie ctasis, lung abscess, empyem a)

2.

Carcinom a lung

3.

Fibrosing alveolitis

Cardiova scular disease 1.

Cyanotic heart disease (Fallot's tetralogy, transpositio n of great arteries)

2.

Infective e ndocardit is

Gastroin testinal tract disease 1.

M alab o rption syndrome

2.

Crohn's disease

Fig. 2.10: Pitting of nails

Fingers Osier's nodes: These are pea size painful swellings in the pulps of terminal phalanges. These are seen in infective endocarditis and are due to vasculitis. Heberde n's nodes*: These are bony swellings on the side of te rminal interphala ngeal joints,

*

Bouchard's nodes: These are similar to H eberden's nodes and occur at proximal interphalangeal joints (Fig. 2.1 lB, 2.12).

Chapter 2- Physical Examination

~7

are osteophytes seen m osteoarthritis (Fig. 2..' 1 . 2. 12).

B

A

f ;. 2.11: N odes in the fingers (A) H ebe rden 's (B) uchard's

Fig. 2.13 : Rhe umatoid arthritis: swollen proximal interphalangeal join ts

• Heberden's node

Button-hole deformity (fixed flexion at proximal interphalangealjoint and extensio n at terminal interphalangcal joint - Fig. 2.14A). Button-hole deformity

Bouchard's node

(

A

Swan neck deformity

f:,;. 2.12: O steoarthritis; H e berde n's and Bo uchard's i1

es

Joint swelling/deformity: In rheumatoid arthritis ? roximal interphalangeal joints are swollen and ri ngers become spindle shaped (Fig. 2.13). In o ng standing rheumatoid arthritis fo llowing efo rmitics can occur.

•

Anterior subluxation of the m etacarpophalangeal joints w ith ulnar deviation (Fig. 2.14B).

•

Swan neck deformity (hyperextension at proximal inte rpha langeal j o int and fi xed flexion at the distal interphalangeal joint Fig. 2. 14A).

·B

Fig. 2.1 4 : Rheumatoid arth ritis (A) button-hole and swan neck deform ities (B) ulnar deviatio n

18

•

'Z ' deformity of th umb.

Arachnodactyly: It m eans fingers are thi n and long, and are seen in Marfan 's syndro me. Palm Pallor: Cola r of palmar skin becom e pale in a11el/lia. Palmar erythema: Rednes of the thenar and hypo thenar eminences is cen in some no rmal subjects. It is al o a feature of hepatic fa ilure, pregnancy, rheumatoid arthriti and o ral contraceptive therapy.

Sweating: Excessive sweating on the palm m ay be idiopathic but is also seen in anxiety (palm is cold) and thyrotoxicosis (palm is warm). Dupuytren's contracture: There is thickening of the palmar fascia felt as th ickened plaque or cord between palm and ring and little fingers. Later, fl exion contracturc of the fi nger , particu larly ring and little fingers may develop. It is a fea ture of alcoholic cirrho i . Pulse Detailed examination of pulse is di cus cd un der card iovascular system. In G PE its rate and regu larity should be noted.

• Blood Pressure Yo u mu t measure the blood pre ure in every patient. So m e doctors prefer to mea ure it du ri ng ge neral physical exam inatio n w hile o the rs do so at the end of examination . It doesn' t make any d ifference as long as measuring the blood pressure isn't fo rgotten . Techn iq ue i discussed under cardiovascu lar system exam inati on (page 38).

ushing synd rom e, xanthclasmas, Facies of exophthalmo , butterfly ras h, and h ir uti m arc comparative ly uncommon.

Common signs to be looked for on the face • Puffi ncs • Pallor of the lower co njunctiva • Yellow discolo ration of the sclera • Blui h di coloration of the tip of the nose and ear lobules • Blui h di colo ration of the inner surface of the lower lip • Dryness, pallor and cyanosis of the dorsu m of the to ngue • Yellowness of undersurface of th e to n ue General appe arance: T h ere are certain characteri tic fac ies, e.g., m oonlikc face o f C11sl,i11g's sy11drol/le, masklike (e:xpressio n le s) face of Parki11so11is111. Puffiness: This is d ue to periorbital edcm a and is ee n in renal failure, 11ephrotic sy11dro111e and awte glo111emlo11epl,ritis. It m ay also be d ue to angiocdema and myxed ema. In right heart fail ure pu ffi ne of the face is uncommon and o nly occurs if pati ent can lie flat. means It (exophthalmos): Proptosis protrusion of the eyeball. If eyes look un usually prominent, inspect them fro m above. Stand behind the catcd patient, d raw the upper lids gently upward, and note the relatio nship of the corneas to the lowe r lid s. If cornea is protruded beyond the lowe r lid exophthalmos is present. In Grave's disease exophthalm os is usually bilateral, altho ugh it m ay be unilateral initially. O rb ital tumo r is another cau e of unilateral exophthalmos. Other eye signs of G rave's d i case are lid retraction* and lid lag*"*.

Face ommo n physical signs w hich mu t be looked for o n the face are puffiness, pallo r of the lower conjunctiva fo r anemia, yellow di colo ration of the clcra fo r j aundice, blui h di colo ration of the tip of the nose and ear lobule fi r cyanosis, b lui sh discoloration of the inner urface o f the lower lip for cyanosis, d ryness, pallor and cyano is of dorsum of the tongue and yellowness o f the under urface of the to ngue. \

*

Lid rerractio11 : Ask the patient to look traight. Norm ally clera above and below the cornea i not visib le. In thyrotoxicosis sclera above th e corn ea may be vi ible due to lid retraction w hile in marked proptosis sclera, bo th , above and below th e cornea is visible. ** Lid lag: A k the patie nt to look straight at your fi nger and then fo llow it downwards. N orm ally both eyeball and upper eyelid m ove together w h ile in thyrotoxicosis u pper eyelid may lag behind.

Chapter 2- Physical Examination

Xanthelasmas: These are yellow plaques on _ ·el id due to depo ition oflipids. These may be -5.SOCiated w ith hypcrlipidemia, but are also seen elderly w ith normal lipids. C olor of the conjunctiva: Ask the pati ent to k upwards, pull the lower eyelid downwards - expose the conjunctiva (Fig. 2.15) and look · r pallor. Subconj un ctival hcmorrhage arc : n a bright patches on the eyeball and occu r , chout any cause but may be due to trauma or :-'eeding disorders.

19

Rash: In systemic lupus erythematosis, there is rash over the cheek and bridge of the nose (butter fly rash) . Color of skin: Bluish discoloration of tip of the nose and car lobules occurs in cyanosis. Redness on the checks (malar flush) may be due to mitral stenosis, but may be seen in normal individuals too. Hirsutism: There is excessive growth of hair on face (moustache and beard area), limbs and trunk in a female. Parotid glands: Swelling of parotid glands may be due to mumps (usually bilateral) or tumor (unilateral). Lips: Pull the lower lip and look for bluish discoloration ofits inner surface due to cyanosis . Aphthous ulcers (yellow base w ith red hallow) also occur on inside of lips. Tongue: Look for dryness (which is seen in d ehydration and mouth breathers) , pallor and cyanosis on the dorsum of the tongue. Other signs include baldness due to atrophy of villi, redness due to inflammation and white patches due to candida infection.

f,::. 2. 15: Exposure o f the lower conjunc tiva fo r pallor

Color of sclera: Ask the patient to look downward s and pull the upper eyelid upwards Fig. 2.16). Normal sclera is white. In jaundice u becomes yellow.

Look fo r jaundice on the undersurface of the tongue. Look for size of th e to ngue (tongue is enlarged in am yloidosis and acromegaly).

Neck Examine the neck for: •

Thyroid

•

N eck veins

•

Lymph nodes

Thyroid It consists of two lobes lying on either side of the trachea and connected to each other by the isthmus. Enlargement of the thyroid is called go1ter. Inspection

Fig. 2. 16: E:-..'Posure of the upper sclera for jaundice

Ask the patient to e>.'tend the neck and look for obvious swelling on either side of the trachea or in front of it. Ask the patient to swallow. Any

20 swelling that moves up with laryngeal cartilage on deglutition (swallowing) is enlarged thyroid. N o te its size, w hether it is unilateral o r bilateral, diffuse o r nodular.

Palpation It can be carried out, both, fro m fro nt and back (Fig. 2. 17). Put bo th your hands over the swelling and palpate . Ask the patient to wallow and note various ch aracteristics a swelling m oves under your fin gers. N ote:

Neck Veins Examinatio n of pu lsation in the jugu lar veins give a nearly acc urate estimation of the right atrial pre u rc (which is also called j ugular veno us pressure o r central ven o us pressure). Examine the patient fro m right side w hile head of the bed is elevated about 45 degrees. Look fo r veno us pulsatio ns in the internal j ugular vein alo ng the anterio r border of the stcrnomasto id and m easure vertica l di tancc from the highest point of veno us pul atio n to the sternal angle. If it is m o re than 3 cm it is abno rmal. More details arc given o n page 40.

Lymph Nodes Lymph nodes of the neck arc divided into fo llowing grou p (Fig. 2.18) :

Fig. 2. 17: Palpatio n of thyroid from behmd

•

IZC

•

Diffu c, single nodule o r multiple no dule

•

Consi tency

•

Tenderness

Retrosternal thyroid. Thyroid can be partially or totally retrostcrnal and in th is case its lower limit cann o t be reached . When patient i a kcd to raise the arms above his head , there i strido r, face is congested and neck veins becom e diste nded ; this is called Pe111berto11 's ign.

Auscultation A bruit (a sound resembling murmur, see page 37) may be audible if thyroid i hyperfunctio ning. k the patient to hold his breath while auscultating for thyroid bruit w ith the bell. It sho uld no t be confused w ith murmur radiating fro m heart, carotid bruit or venous hum (page 57).

Fig. 2. 18: Lymph nodes groups in the neck

• •

Submc ntal (under the chi n)

•

Pre and po tauricular

• •

O ccipital

•

Lymph nodes of anterio r triangle in fro nt of the ste rnomasto id

Submandibul ar (unde r the j aw)

Lymph node of posterior triangle beh ind the stcrnomasto id

Method of Palpation Stand behind th e patient, flex his neck and push middle and ring finger of both h ands under the chin. Move th e fingers backwards to palpate

Chapter 2- Physical Examination

snbmental and submandibular groups. Then - pace in front and behind the auricle and over e occipu t. M ove your fingers downwards hind the sternomastoid cowards clavicle - r lymph nodes of posterior triangle. For _ pation of supraclavicular fossa, push your - gers behind the clavicle (Fig. 2.19). Fina lly, \·e the fingers upwards between trachea and momastoid for lymph nodes of anterior m angle.

Rig t

21

ilia

Elevate patient's arm above his head and push fingers of the left hand up in the ax:illa, palm facing patient's chest. Bring back patient's arm alongside his chest. Move your fingers downwards along the chest wall. Iflymph nodes are enlarged, they will slip between your fingers and patient's chest (Fig. 2.20). Elevation of patient's arm is necessary to reach the apex of the axilla. In this way apical, central and medial groups are palpated.

- :- .2 .19: palpation of supraclavicular lym p h nodes Fig. 2.20: Palpatio n of righ t axillary lym ph nod es

_ -ore the following features if lymph nodes are :."alpable: •

Site

•

Size

•

Number

•

Consistency

•

Mobility with reference to each other (matted or discrete), to overlying skin and to underlying structures

•

Tenderness

•

Discharge or sinuses

Lvm ph nodes are tender in acute infection, m atted together in tuberculosis (sinuses may also be present), discrete and of rubbery consistency in Hodgkin's disease and hard in consistency in m etastases .

_-\.xillary Lymph Nodes T here are six groups: anterior, posterior, lateral, medial, central and apical.

For palpation of anterior group, hold anterior axi llary fold between thumb and fingers of your left hand. For lateral group, place palmar aspect of finge rs of your right hand along the medial side of the humerus. For posterio r groups of both sides, hold posterior axillary folds betvveen thumb and fingers of your corresponding hand from behind the patient.

When a group of lymph node is palpable, examine its drainage area.

Left Axilla Same process is repeated but apical, central and medial groups are palpated with the right hand (Fig .. 2.21) w hile lateral group is palpated with the left hand.

~

--

~ - - -- - - - -- - -- - - - - - -- - - -- -

22 Feet Look for c lubbing, koilonychia and cyanosis in the feet as well. Feet arc common ly affected by ischc mia due to pe ripheral vascu lar disease; early signs are loss of hair and shiny skin.

Edema Look for ed e m a over the dorsum of the foot, be h ind m edial m alleolus and over the shin. In a Fig. 2.2 1: Palpation of lcfr axi llary lymph nodes

Epitrochlear Lymph Nodes These are palpated by the method shown in Fig. 2.22.

bedfast patien t also check over the sac rum. Compare two sides. Prcs the thumb fo r at least 5 seconds. If cdc m a is present, a pit is fo rmed which re fill s g rad ually. In cardiovascular conditio ns, edcm a is more prominent in lower half of the body. In hypo prote inemia, there is generalized ana area and pitting can be d emonstrated over the upper half of the body as well.

Causes ofedema Pitting edem a Generalized/bilate ral A. Fig. 2.22: Palpatio n of epitrochlear lymph nodes

Lymph Nodes of Groin These arc easily palpable over the inguinal ligament, if enlarged . Isolated e nlargement of this group is less significant compared w ith o ther groups.

Note Lymph nodes are commonly enlarged due to disca e of the drainage area, e.g., infectio n o r malignancy. So w he n you detect an enlarged lymph node, examine the drainag e area of that lymph node to exclude any pathology. Examine scalp, face and oral cavity in case of cerv ical lymph nodes, uppe r limb in case of axillary lymph nodes and lower limb in ea e of inguinal lymph nodes.

Causes ofenlarged lymph nodes 2.

Infectio n o r malignancy in drai nage area Tube rculosis

3.

Lymphomas

4.

Lcukemias

1.

Cardi ovascular (only in the lower half of the body) 1.

Rig ht heart failure

2.

Constrictive pericarditis

3.

Pe ricardia( effusion

4.

Infe rio r vena cava obstruction

B . Re nal (generalized but more on the face) 1.

Renal failure

2.

Nephrotic y ndro m c

3.

N ephritic syndrome

C. Hypo protcinemia; other tha n nephroti c syndrome (ge neralized) 1.

Cirrhosis of live r (decreased synthe is of albumin)

2.

Malnutrition

3.

M alabsorption

Localized (only in the affected part) 1.

Ven o u ob tructio n

2.

Immo bil e, bedridden patient, e.g., paralysis

3.

Inflammation (e .g., ccllulitis)

Chapter 2-Physical Examina tion

_ -on-pitti ng edema* .._ Lympha tic obstruct ion 1. Fi lariasis M ilroy's syndrom e ? 3.

urgical removal /irradiat ion of lymph nodes

B. Angioed em a C. Myxcde ma - rate of Hydrat ion • de hydratio n (loss of fluid from the body):

•

• •

• •

Eyes are sunken . There is dryness of tongue . decrease d. (It is i demons trated by pin ching a fold of skin between thumb and fi ngers; it will subside abnorm ally slowly. In elderly, this sign is le s reliable.) Pulse i rapid and blood pressur e is low; there is postural hypo tensio n.

Skin

elastici ty

Urine output is decrease d .

Respira tory Rate hould be counted for full minute countin g abdomin othoraci c m ovem ent . N ormal rate i 14 - 16/minu te.

Temper ature Thermo meter can be placed at va rio us site fo r reco rding the body tempera ture, e.g., under the rongue, in the axilla, groin or rectum. M outh o r ax:i lla is the usual sites. The rectal tempera ture 0.9°F higher than the oral tempera ture 1 w hich in tu rn is 0.9°F higher than the axillary cempera ture. Rectal readings are m o re reliable chan o ral or axillary read ings. N o rmal average o ral te mpe ratu re is 98.4°F (98°F - 99°F) w ith a variation of l .0°F betwee n m o rning (low) and evening (high) (diurna l variatio n).

Patient should not have taken hot or cold

*

A part of the body looks swollen (veins, tendon s and bone~ are obscured ) but there is no pitting on pressure. Jc should be d ifferentia ted from obesity in w hich skin is normal and foot (hand in case of upper limb) is spared whi le in non-pitti ng edema skin 1s chickened and foo t (or hand) is swollen coo.

23

drink immed iately before recordi ng oral temper ature. Thermo meter shou ld be shaken wel l below 98.4°F and left in place for 1/2 - 2 minutes (a little longer than the manufacturer instructi ons).

Pallor Anemia (reduced hemoglo bin concentration) is the most common cause of pallor. Vasocon striction (as a result of shock, heart failure and e2'.'])0Sure to cold or Raynaud 's phenom enon) and hypopitu itari m are o ther causes. It should be looked for at fo llowing ites: N ails Palmar skin • Lowe r conjunc tiva • Dorsum of the tongue Vasodila tation may deceptively produce pink color in the resence of anemia. • •

Cyanos is**

If the concent ration of reduced hemoglo bin in blood rises above 5 gm %, a bluish tinge is seen in the skin and mucous membra ne; this is called cyanosis. Sites to look fo r cya nosis arc : • N ails • Tip of the nose • Ear lobule • Inner surface of the lip •

Tongue

Periphe ral cyanosi s If only nails, nose and ear lobules are cyanosed w hile the color of the li ps and to ngue is normal, it is called peripher al cyanosis. It is due to, either reduced blood suppl y or defective veno us drainage. The hands arc usua lly cold in this conditio n.

Causes 1. 2. 3.

**

Exposur e to cold Severe hypotension Raynaud 's pheno m eno n

Bluish discolo racio n al o occ urs due co sulfhemo globin and m cchcm oglobin w hi ch arc abnorma l pigments formed as a res ult of exposure co certain drugs or toxins. The pacicnc is not breathles s. Oxygen sa turatio n ofhem oglobin is normal. Diagn osis is made by spectrosc opic examinat io n of blood .

24 4. Ven ous o bstruction Central cyanosis If lips and tongue are also cyanosed , it is called central cyanosis. It may be due to the inability of the lungs to oxygenate the blood, o r the mixture o f venous blood w ith arterial blood in the heart o r outside. Patient is usually dyspneic. Causes 1. Re piratory failure (page 91) 2. Cyanotic heart diseases (Fallot's tetralogy, transpositio n of great arteries, Eisenmen er's s ndrome

In cirrhosi , the pubic hair distribution becomes fe male type in male patients, and there is loss of axillary hair. In certain endocrinal disorder , there is hirsutism (hair growth on face, trunk and limb of a female).

Jaundice Bilirubin is the end product of hemoglobin metabolism . When its concentration in the serum rises above 2 mg%, it becom es clinically detectable as a yellow discoloration of various tissues and is called jaundice. It sho uld be looked for in bright day light as mild j aundice may be missed in artificial light. Sites to look for jaundice are: • Skin • Sciera (most reliable site) • Undersurface of the tongue Jaundice should be differentiated from an uncommo n condition called hypercarotenemia which occurs in people who eat excessive quantities of carrots. Skin is yellow but sclera is w hite.

Generalized greyish-bronze color pigmentation is a fea ture of hcm ochromatosis.

Subcutaneous Emphysema C rackling sensations are felt w hen the affected skin is palpated. It is due to leakage of air fro m the chest as a result of penetrating chest inj ury, accidental injury to the lung during thoracic paracentesis, escape of air during intubation of chest for pneumothorax or rupture of esophagu s. It is also present in gas gangrene.

Hair Distribution There is characteristic distribution of hair in male and female. In fe m ale pubic hair are limited to the pubic area with h orizontal upper border w h ile in m ale they spread further up the abdom en towards the umbilicus in a triangu lar pattern.

Pigmentation In Addison's disease (decreased productio n of cortisol by adrenal glands), there i dark brown pigmentatio n of c>qJosed parts, axi llac, palmar crease and recent scars. A bluish black pigm entation is also seen in buccal m ucosa but it may be normal in N egroes.

M ask-like pigmentation (also called chloasm a) occurs in pregnancy (it may occur in women taking estrogen containing contraceptive pi lls).

Cafe au lait spots: These are brow n patches of pigmentation seen in patients of neu rofibromatosis. Albinism: There is congenital absence of melanin pigment w hich is generalized . Vitiligo: There are patches of w hite and darkly pigm ented skin. It is associated w ith autoimmune disorders. Abnormal Sounds and Odors Strido r is an inspiratory w histling sound heard in upper respiratory tract obstruction. Wheeze is similar sound but occurs in expiration and is due to spasm of smaller airways. In hepatic failure there is a sickly odor in the breath of the patient and is called fetor hepaticus. In ketoacidosis there is a sweat smell of aceto ne in breath. In renal failure there is fishy or ammoniac sm ell. In gastric outlet obstruction there is fo ul sm elling belching.

Halitosis o r bad breath is very disturbing for the patient. Its causes include gingivitis, stomatitis, atrophic rhinitis, tumo rs of nasal passage and suppurativc lung diseases. Definitions of Skin Lesions Macules: T hese are areas of skin discoloration w hich arc neither raised nor depressed . Papules: These are elevations of skin w hich are

Chapter 2-Physic al Examination

25

-:- pable and diameter is less than 5 mm. _ -odules: These are similar to papules but .:....:meter is more than 5 mm.

Hematom a: It is palpable fluctuant collection

,-e- ides: These arc cystic swellings contai ning rou fluid and diam ete r is up to 5 mm. Pustules : These are similar to vesicles but fluid o paq ue and yellow.

dilated sm all blood vessels.

Bullae: These arc cystic lesio ns of m o re than

5 mm diamete r and arc fill ed w ith serous, "rop urulent o r hcmo rrhagic fluid . ~ eals: T hese arc swellings of skin due to acute xalizcd edcma. - les: These are formed by ab normal .: · eq uamation o f supe rficial layer of skin . Crusts: These arc formed by dried secretion s.

Purpura: It means bleed ing into the skin. Petechia e: These are red lesions 1 - 3 mm .:1ameter due to bleeding and do n't blanch o n :-re urc. Ecchymo sis: T hese arc large reddish blue -ions due to bleeding into subcutan eous tissue d arc also ca lled brui cs.

o f blood.

Telangie ctases: These arc groups of abno rmally Spider nevi: These consist of a central arteriole from w hich cveral branches radiate. When the central arterio le i obliterate d by p ressure with a needle, all the branches are blanched and refi lling starts fro m the ccntcr w hen needle is removed.

C ampbell de Morgan spots: These are red swe ll ings, ·1 - 2 mm in di ameter w hi ch don't fade o n pressure and commo nl y develop o n chest and abdomen w ith adva ncing age.

Erythem a nodosum : There are red, painful, te nder, induratcd swellings of va riable size (from few millimetc rs to several centimetc r ) mainly on the shin. Common ca uses arc primary tubcrculo si , streptococca l in fec tio n, sarcoidos is and drugs .

Erythem a margina tum: These arc transient pink patchc m ainly on the trunk w hich j oin to form large areas w ith pale centcr, and arc o ne of the m ajor criteria of rheumati c feve r.

U MMARY OF GENER AL PHYSIC AL EXAMI NATION --

General appeara nce

Youngor old H ealthy or ill

Physique

Normal Unusuall y rail or ho rt Obese, thin or wasted

Consciou sness

Puffy Alert and o rien red Confused Drowsy

Posture and attitude

Un conscio us (test con cious level using G lasgow coma scale) Comforta ble D yspneic

In pain

Hand

Shape

Lyi ng in the bed Lying propped up Sitting up and bending fo 1ward Lying still Writhing in the bed Short m etacarpals 1 Carpal spasm

26 Nails

Size Pallor

N ormal or broad

Cyanosis Koilonychia C lubbing Splinter hem orrhages Leuconychia Pitting of nails

Fingers

H alf and half nails O sier's nodes

l

I

H eberden 's nodes Bouchard's n odes J oint swelling Deformity of fingers

Palm

Arachnodactyly Pallor Palmar crythem a

I

Sweating

Pulse Blood pressure

Dupuytren's contracture Rate and rhythm Palpatory method

Face

Auscultatory method General appearance

I

I

I I

I

M oonlike face

I

Expressionless face Puffiness Proptosis Xanthelasmas Colar of lower conjunctiva Cola r of sclera .I

Rash Cola r of skin Hirsutism Parotid glands Lips Tongue

D ryness (dorsum of tongue)

I

Pallor or cyanosis (dorsum of tongue) Yellowness (undersurface)

Neck

Thyroid

Size Inspection Palpation Auscultatio n Pemberton's sign

I 'I

:1

II j

Chapter 2- Physical Examination N eck veins Lymph nodes

(11ote characteristics ifpalpable)

Venous pulsations ' Level of jugu lar venous pressure Submental Submandibula r Pre and postauricular O ccipital

_.\xilla

Lymph nodes (note characteristics ifpalpable)

Posterior triangle Anterior triangle Ante rior Posterior Lateral M edial Cen tral Apical

Groin Feet

Lymph nodes C lubbing Koilonychia Cyanosis Loss o f hair

Edema

Edema D orsum of foo t Behind m edial m alleolus Shin

Respirato ry rate Temperature

Sacrum (bed fas t patient only) Count fo r full m inute Keep the therm ometer 111 the m o uth, axi lla or groin longer than recommended by the m anufacturer

Pi tting N on-pitting

27

28 WRITING OUT ROUTINE EXAMINATION An ill looking old man lying in the bed. He is of normal height and built and fully con cious.

•

Pulse: 84/ minute

•

BP: 162/94

• Re piration: 24/ minute • Temperature: 100.2°F • Pallor: absent • Cyanosis: absent • J aundice: absent • C lubbing: absent • Koilonychia: absent • Splinter hem orrhages: absent • Leuconychia: absent • Osier's nodes: absent • H eberde n' nodes: absent • Bouchard's nodes: absent • Interphalangeal j oints: normal • H and deformity: absent • H and size and sh ape: no rmal • Palmar sweating: ab ent • Palmar erythem a: absent • Dupuyn en 's contracture: absent • Facial appearance: normal • Perio rbital edema: absent

• •

P roptosis: absent

•

Parotid gland: not enlarged

•

T hyroid: diffusely enlarged , nontender, no bruit audible

• •

N eck ve ins: not engorged

Skin rash: absent

Lymph node :

•

Cervical: t v,10 postauricular lym ph nodes palpable, 1cm diam eter, discrete, mobil e, nontender, no discharge or sinus.

• •

&-illary: n ot palpable Inguinal; not palpable

• Ankle edema: present, pitting •

Dehydration: absent

CHAPTER

Cardiovascular System Clinical examination of the CVS (Cardiovascular System) is particularly rewarding as it usually leads to an accurate diagnosis. Investigations are carried out, either to confirm the clinical impression or to differentiate between various possibilities.

SYMPTOMS Early diagnosis of important cardiac diseases like ischemic heart disease and heart failure is based on careful history taking. There are two cardinal symptoms of cardiovascular disease - dyspnea and chest pain.

Major symptoms of cardiovascular disease Dyspnea

Orthopnea In patients of severe heart failure breathlessness worsens on lying flat; this is called orthopnea.

Exertional dyspnea

Pulmonary edema

Paroxysmal nocturnal dyspnea

There is transudation of fluid into the alveoli of lungs and left heart dysfunction is most important cause. Symptoms are persistent severe breathlessness, orthopnea and cough productive of copious, frothy, watery, blood stained sputum.

Orthopnea

Chest pain

Paroxysmal Nocturnal Dyspnea The patient wakes up at night due to severe breathlessness which improves on sitting upright for several minutes, and is usually accompanied by cough and frothy sputum. This is called paroxysmal nocturnal dyspnea. This is due to transient pulmonary edema, precipitated by increased venous return to the heart in recumbent position. It is a feature of left heart failure; causes include left ventricular pressure/ volume overload (hypertension, mitral/aortic valve disease) and severe left ventricular disease (ischemic heart disease, cardiomyopathy).

Ischemic heart disease

Angina Infarction

Pericarditis Dissection of the aorta

CHEST PAIN It is an important symptom of heart dise~se. Its characteristics vary with the underlymg pathology.

DYSPNEA Dyspnea or breathlessness means difficulty in breathing. It may occur on exertion or at re st -

Exertional D yspnea . an early symptom o f hea rt· fiailure · Initially, It 1s ed or strenuous . . It may occur after unaccu st on1 . progre sses , patient may exertion but as disease )king a few steps. ' become breathless even on wa

Jschemic Heart Disease It means the coronary arteries cannot maintain adequate blood supply to the myocardium. It may prese nt as angina or irifarction . Angina Pectoris There is transi ent myocardial ischemia . The patient develops chest pain on exertion which

-

1 ~

--- ---=====- ~

3~0 _ _ _ _ _ _ _

is relieved within minutes by rest and sublingua l nitroglyce rin. Pain is retrosternal, across th e chest and rad iates to the jaw and left arm . Patient describes it as a tight band around the chest or heaviness. It may be associated with dyspnea, palpitation and sweating. Total duration of pain is less than 30 minutes.

Myocardia l Infarction There is total occlusion of one or more branches of the coronary artery and the dependent m yocardium dies. Pain is similar to that of angina pectoris but duration is more than 30 minutes and it is not relieved by sublingua l nitrates or rest. Pericardit is Features are similar to the pain of ischemic heart disease. There is no effect of exercise, rest or nitrates. It is relieved by leaning fo1ward and may get worse on deep breathing and coughing.

Dissection of the Aorta Pain is abrupt in onset, severe in intensity, tearing in character and is felt in front of chest or back between th e scapulae or at both places.

EXAMIN ATION

Wlien you are. asked to examine a part'ICU 1ar

system of a pa~1 en~, always start from the genera] physical e~a~1mat1on except when examiner asks you to omit 1t. Examinatio n of the cardiovascu lar systeni consists of: 1. Examinatio n of pulse 2.

Measurem ent of blood pressure

3.

Examinatio n of neck veins

4.

Examinatio n of precordium by: a.

Inspection

b.

Palpation

c.

Percussion

d. Auscultatio n

EXAMIN ATION OF PULSE The pulse is a wave imparted by the contraction of the left ventricle to the blood column and travels 10 times faster than the blood itself Pulse is felt where an accessible artery can be pressed against an underlying bone.

Pulmonar y Embolism

Commonly felt pulses are radial, brachia!, carotid, femoral, popliteal, posterior tibia! and dorsalis pedis. Pulse becomes impalpable when systolic pressure falls below 50 mmHg in adults.

Peripheral embolism causes pulmonary infarction . Its pain is pleuritic discussed under respiratory system. Major central pulmonary embolism causes pain undistingui shable from pain of ischemic heart disease.

Radial pulse: It is the most easily accessible and the most commonly felt pulse. The patient's hand should be slightly flexed and pronated. Pre~s the radial artery against the head of the radms (Fig. 3.1A).

P recordial C atch It is a transient, sharp pain at the site of the ca rdi ac apex, commonly felt by normal subjects. It has no significanc e. Note: Persistent precordial pain unrelated to the exe rtion , is not due to cardiac di sease.

PALPITA TION It i'> awareness of the heart b eat and is a co mm o n fc;iturc of :rn.x icty. It al so occurs in tac hyo rdi a a11cl hca n f.1ilurc .

Brachia! pulse: Flex the patient's arm and feel f~r the_ tendon of the biceps; press on its medial side with the thumb of your opposite hand (fig. 3.18). Carotid pulse: Place the thumb or fin gers o( your opposite hand along the anterior b0rd cr of th e st ernomasto id at the level of laryngc~I ·1 ' r ) ~arti age and press backwards (Fi a. 3.2). J{cl'f . o I~ 11 ~ mind that carotid sinus (prese nt :it t , b1furcat' ' ion o f con1mon carotid artl'I')' ) n1-''.' be stiniu 1ate d . bra dye,1rd·Js1.1 and can result 111 0 .r syncopy. Don't palpate both carotl . sunulta neous 1Y because blood suppl y co rl1l

Chapter 3-Cardiovascular System

31

~ . l pu lse Fig. 3. 1: Palpation of (A) radial pulse (B) b rac h 1a

I

I

Fig. 3 .2: Palpation of carotid pulse

brain may be critically reduced. Palpate the right carotid from the right side and the left from the left side. Femoral pulse: Press with the thumb/finger halfway between the anterior superior iliac spine and the pubic tubercle along inguinal ligament

A

(Fig. 3.3A).

Popliteal pulse: Popliteal artery lies deep in the popliteal fossa and is difficult to palpate. Flex the knee at an angle of 120° and push fingers of both hands into the popliteal fossa keeping your thumb on the patella (Fig. 3.3B).

Dorsalis pedis pulse: Palpate in the proximal pare of the first intermetatarsal space (Fig. 3.4A). Posterior tibial pulse: Palpate behind the medial malleolus (Fi g. 3.48).

B Fig. 3.3· Palp.1tiu11 of (A) fi.·moral pulse (13) pt)phtcal pulsl'

1 32 3

·

A

Norrn~y R e lative bradycardia: · c Puls , . 10 beats per mmute 1or eacI1 degr e nses in the body temper ee F (or Q.S°C) rise . _ Uu~ If pulse rate IS sloweI than expected ro; the body temperature, it is called relat· !Ve bradycardia.

Rhythm Normally interval betw~en the be~t~ is constant and rhythm is regular (Fig. 3.5). If it Is disturbed pulse becomes irregular. '

L-----~

B

Fig. 3.5: Normal pulse

1.

----

Sinus arrhythmia: Pulse rate is faster during inspiration and slower during expiration (Fig. 3.6). This is a normal phenomenon and is more pronounced in certain individuals. It disappears in heart failure and autonomic neuropathy. Inspiration

Expiration

Fig. 3.4: Palpation of (A) dorsalis pedis pulse (B) posterior tibia! pulse Fig. 3.6: Sinus arrhythmia

During examination of pulse note the following features: 1.

Rate

2.

Rhythm

2.

3. Volume 4.

Character

5.

Comparison with other pulses Condition of the vessel wall

6.

Rate Count the pulse for full one minute. Normal average pulse rate is 72 beats per minute. It is equal to the heart rate except in cert · arrhythmias like atrial fibrillation. am 1.

Tachycardia: It means pulse rate is m . ore than 100 per mmutc.

2.

Bradycardia: It means pulse rate is less than 50 per minute.

[

Occasional irregularity: It is due to premature beats. Premature beat occurs earlier than expected normal beat, is weak and is followed by a longer pause (Fig. 3.7). Occasional premature beats are common in healthy . divi .. d uals and are not significant. F quent m re · · · h nderlying premature beats m a patient wit u heart disease should be taken serioUSly. Ectopic beat I

Fig. 3 .7: Occasional irregularity

3

occllr

· Regularly irregular: Premature beats one at a fixed interval (Fig. 3.8), e.g., after ;11 11 n orma l beat . . (b1gemmy) or tw 0 nofl st 0 beats (trigeminy). Digoxin toxicity is th e fl1 common cause of such arrhythmias.

Chapter 3-Cardiovascular System

33

Causes of Abnormal Heart Rate Tachycardia

Bradycardia

Relative bradycardia

Exercise

1.

Athletes

1.

Enteric fever

2. AIEiety

2.

Complete heart block

2.

Viral infections

I. 3.

Fever

3.

Drugs like digoxin, beta blockers 3.

4.

Anemia

4.

Raised intracranial pressure

5. Heart failure

5.

Hypothyroidism

6.

Hypotension

7.

Thyrotm,'i.cosis

8.

Tachyarrhythmias (e.g., supraventricular tachycardia)

Meningitis with raised intracranial pressure.

Volume of Pulse

Fig. 3.8: Regul arly irregul ar pulse

Irregularly irregular: There is no pattern and beats occur irregularly (Fig. 3.9). It is easier

4.

to detect if rate is fast.

This is the amplitude of the pulse wave and is determined by the amount of displacement of the palpating fingers. Pulse could be of normal volume (learned by experience), high volume (e.g., fever, aortic regurgitation) or low volume (heart failure)

hypovoleniic shock).

Fig. 3 .9: Irregul arly irregul ar pulse

In younger people it reflects stroke volume. In old age vessel wall becomes rigid and pulse volume is higher than expected for the stroke volume.

Causes of irregularly irregular pulse

Character of Pulse

1.

Atrial fibrillation

2.

Frequent multiple premature beats

3.

Atrial flutter with varying block

In certain diseases the pulse wave has a specific wave form or character. A major pulse close to the heart (brachia!, carotid, femoral) should be palpated for this purpose.

Pulse deficit: In atrial fibrillation some of the left

1.

Slow rising pulse (pulsus plateau): It is a low volume pulse, rises slowly and stays longer with the palpating finger (Fig. 3.10). Pulse pressure is narrow. It occurs in aortic

ventricular contractions are weak and are not conducted to the arteries; the pulse rate is slower than the heart rate counted by auscultation. The resulting difference between pulse rate and heart rate is called pulse deficit.

stenos is.

Causes of atrial fibrillation 1.

Mitra] stenosis

Fig. 3. 10: Slow risin g pu lse

2.

Thyrotoxicosis

2.

3.

Ischemic heart disease

4.

Hypertension

Collapsing pulse (water l,ammer pulse): It is a high volume pulse with no rmal upstroke but rapid downstrokl' (Fig. 3. 11).

l 34 . , _· Grasp the pati ent s WI 1st w ith your . right fi 1 . d · ) pulse 1s e t palm in such a way t I1at ia ia . alono- metaca rpop I1a Iangea I promm ences. . . g Lift :::,the patient 's arm su dd en 1Y bY graspm .l . c. h nd (not wit 1 his fingers with your 1eit a . . · . ·ent mcreas ed the no-ht hand) T 11ere is tJ ans 1 run-of f of blood toward s heart due to effect of the o-ravity and collaps ing charact er of the pulse become s more obviou s for a few beats.

cardiac tampo nade

Bronchial asthma

Fig. 3.14: Pulsus paradoxus

Fig. 3.1 I : C oll apsing pulse

3.

The collaps ing pulse reflects wide pulse pressu re (>60 mmHg ). Aortic regurgitation is the most import ant cause, but it can also occur in ventric ular septal defect, persiste nt ductus arterios us, severe anem1a and arterio venous fistula. Pulsus bisferiens: Two systolic peaks are palpabl e in one pulse. (In dicrotic pulse 2 nd peak is in diastole. It is not palpable and is only seen on direct recordi ng of the pulse) (Fig. 3.12). It is someti mes seen in combined ao11ic stenosis and regurgitation .

Fig. 3. 12: Pulsus bisferie ns

4. Jerky

pulse: In hypertrophic obstructive cardiornyopathy ejection of blood is normal initially. It i~ then sudden ly obstruc ted by th e contrac tion of a band of muscle in the aortic outflow tract. It gives a jerky charact er to the pulse (Fig. 3.13).

Fi g. 3. 13: J crl·y ptilse

5.

]

P11/sus paradox11s: Pulse either b . . wea k or tmpalp ablc during in spir , t. ccomcs T . . . a 1011 . his 1s a n exagge ration of a n o rm a l pi 1 cno1nc1 1 (Fig. 3. 14) . 011 L

Norma lly, during inspira tion there is a fall in the systoli c pressu re, about 5 mmHg or less; in pulsus parado xus this fall is more than 10 mmH g. It occurs in massive pericardi a\ effusio n (cardiac tamponade), constnctwe pericarditis and acute severe bronchial asthma. Pulsus parad oxus * can be confirmed by checki ng the blood pressur e during inspira tion and expira tion. Ask the patient to breath quietly . Inflate the cuff above systolic level and then deflate it gradually. Note the level at which Krotok off sounds first appear. These will be audibl e during expiration only. Contin ue deflati ng the cuff till the sounds remain audibl e throug hout respirator)' cycle and note this level as well. In pulsus parado xus differe nce betwee n these rwo levels is more than 1O mmHg . 6- Pulsus alterna ns: A strong beat alternates with a weak beat but the interval between beats is consta nt ~nd rhythm is regular (Fi~ 3 · 15) - I t 1s · seen in left ventncu · /ar fiar·tore an suprav entricu lar tachyca rdia.

*

In

d" car 1ac tampo nade only sys to lic. . i> rcss11rr 11 \i' d ec reases· . ,d ;111d P[lotIl · , d.tasto 1·1c rema ms unc I,angl prcs s ure is reduced . In bronch ial a it1:l_ jol1 systo lic d d. . . · 111sr 1r·11 :in 1:istolic pressur es fall durill !:; . J 1~)and puls , . , (fl''· · ·. , . . c pressu re rema ins u11ch:in geL ::,I r.ttl' 1 1its i s d , . Uc to marked ch:inge s 111 t IlL, ·11,rrar111 prcs s urc whi ch arc transmi tted to th e vessels.

sth

J

Chapter 3-Cardiovascular System

!\ Fig. 3.15: Pulsus alternans

Level of systolic pressure is high for strong beats and low for weak beats; this helps in confirming the presence of pulsus alternans by using BP apparatus. Inflate the cuff above systolic blood pressure level as determined by the palpatory method. Lower the pressure in the cuff gradually; at first Krotokoff sounds for strong beats will appear. Note th~ number of these Krotokoff sounds per mmute. Further lower the pressure in the cuff When level of systolic pressure for weak beats is reached, the rate of Krotokoff sounds will suddenly become double. This phenomenon will confirm presence of pulsus alternans. 7.

Pulsus bigeminus: It is similar to pulsus alternans, but interval between beats is variable. A strong beat and a weak beat occur close to each other followed by a long pause (strong and weak beats are coupled), and this cycle is repeated (Fig. 3.16). Strong beat is a normal beat. Weak beat is a premature beat which occurs earlier than its expected time, and is followed by a compensatory pause. Diagnosis is confirmed on ECG which shows ventricular bigeminy. Digoxin toxicity is the most important cause.

Fig. 3.16: Pulsus bigeminus

Comparison with other Pulses Palpate corresponding pulses of both sides simultaneously and compare their volume except carotids. Don't palpate both carotids simultaneously (see page 30). Compare radial and femoral pulses; in coarctation of the aorta,

35

femoral pulse is weak and delayed as compared to radial pulse (radiofemoral delay) (Fig. 3.17). Radiofemoral delay is the most important clinical feature of the coarctation of the aorta.

Fig. 3.1 7: Looking for radiofemoral delay

Condition of the Vessel Wall Feel the radial pulse with three fingers. Press with the proximal finger so that the pulse is occluded and feel the vessel wall with the middle finger. Normally it is not palpable. In advanced atherosclerosis it can be felt as a cord between finger and underlying bone.

' 36 Characteristics of Pulse Characteristics Exampl e • T:1 chycardia Rate

•

Bradycardia

-

Causes

Descrip tion • • Pulse rate more than • 100/ minute

•

Pulse rate less than SO/ minute

Exercise Anxiety

• •

Anemia

•

Heart failure

•

Hypoten sion

• • • • •

Thyroto xicosis

•

Fever I

I I

Tachyar rhythmi as Athletes

I

Comple te heart block

I I

Drugs (digoxin, beta blockers )

I

Raised intracranial pressure I

•

Relative bradycardia

• Pulse rate is less than • expected for body • tempera ture

Rhythm

•

•

• I I I

• •

•

Regular Sinus arrhythmia

• •

Occasional irregularity in pulse

•

Regularly irregular pulse

•

Irregularly irregular pulse

•

Pulsus deficit

•

Viral infection s Mening itis with raised intracra nial pressure

I

I

Interval between the beats is constant

•

Pulse rate is faster during inspirati on and slower during expiration

•

It is a normal phenomenon and is absent in: \

• • •

Heart fai lure

It is due to

Irregularity comes at regular intervals No regularit y at all

Heart rate is faster th an pulse rate and it is the differen ce between the two

-

Normal

I J

occasional prematu re beats

•

Enteric fever

autonom ic neuropathy Commo n in healthy persons

I

• •

Any myocard ial disease

• • •

Atrial fibrillati on

Digoxin toxicity

I

Multipl e ectopics . . h varyinr; Atnal flutter wit · blocks

•

Atrial fibrillation

•

Causes

•

Mitral stenosis

•

Thyroto xicosis

•

. . -·1sc lschcmi c heart d isc,

__• _ Hyperte nsion _

I

---

37

Chapter 3-Cardiovascular System

Characteristics Example Volume

•

Nonnal

•

It is learnt by practice

•

Low volume pulse

•

Pulse is weak

High volume pulse

•

•

Character

Description

Pulse is bounding

Causes

• •

Heart failure

• • • •

Fever

•

Slow rising pulse •

Low volume pulse, • rises slowly and stays longer with the finger

•

Collapsing pulse •

High volume pulse with normal upstroke but rapid downstroke

•

Pulsus bisferiens •

•

Pulsus paradoxus

•

•

•

Pulsus alternans

Two upstrokes in one beat

Hypovolemic shock

Severe anemia Aortic regurgitation Pregnancy Aortic stenosis

• • •

Aortic regurgitation

• •

AV fistula

•

Combined aortic stenosis and regurgitation

Pulse becomes weak • or impalpable during • inspiration

Ventricular septa! defect Persistent ductus arteriosus Severe anemia

Cardiac tamponade Constrictive pericarditis

•

Acute severe asthma

A strong beat alternates with a weak beat and the interval between them is constant

• •

Left ventricular failure S upraventricular tachycardia

•

Pulsus bigeminus

•

Strong and weak beats are coupled and are followed by a longer pause

•

Digoxin toxicity (ventricular bigeminy)

•

Radiofemoral delay

•

Femoral pulse is delayed compared with radial pulse

•

C oarct:1tio11 of :1ort:1

I

I Comparison

with other pulses -

-

-

-

J

38 MEASUREMENT OF BLOOD PRESSURE The Blood Pressure (BP) is the product of · 11eia ·1 the heart rate, stroke volume and penp resistance. There are two levels - systolic and diastolic. There are two types of blood press ure apparatuses (sphygmomanome ters) in common use. In M ercury Sphygmornanomet er a column of mercury moves up and down in a calibrated vertical glass tube as the cuff is inflated and defl ated (Fig. 3.1 8). In Aneroid Sphygmomanomet er a spring is connected to a needle; when the pressure in the cuff changes, this needle moves on a dial and indicates pressure (Fig. 3.19 A). This is less reliable and should be frequently compared with a m ercury sphygmomanometer. In digital blood pressure apparatus there is display of blood pressure on a screen (Fig. 3.19 B) . Cheap versions are not reliable.

Fig. 3.19 B: Blood pressure apparatus; digital type

Method Patient should be resting and relaxed, sitting or lying. Place the manometer at the same level as cuff on the patient's arm (this is not necessary if aneroid type of sphygmomanome ter is used). The cuff should be wide enough to cover about two thirds of the arm length. Higher reading is obtained if a small cuff is used. The length of the cuff should be about 80% of the circumference of the limb and width should be 40% of the circumference of the limb (Fig. 3.20) A standard adult cuff is 12.5 cm wide. In children smaller cuffs are used.

Fig. 3.18: Blood pressure apparatus; mercury type ::t::: ::,

u

Length

Fig. 3 20· BI 00d

pressure apparatus cuff; k nbrt I1 1·s. equall to 80% of the limb's circumference, wid th ,s equa to 40'¾0 0 f I . ' t 1e limb s circumference Remove 11 11 -nII· t e clothing from the upper ·1 Apply theac ff I . •uch .1 LI c oscly to the upper an11 in 5 way that its I 2 5 en• is not less than · J1r: (1") above thowerbborder " • ·• on t nicd "· l . c cu ttal fossa and tublllg 1s 1,1 side (Fig. 3.21). ·

fi~. 3.1pace close to tlic st . . . • tnnu 11 In further d1!>CU!t!tlo11 aortic area w1·11 · . nIcan A unless mentioned othcrwil>c. 1

Fig. 3.39: Areas of auscultation

Method of Auscultation Auscultate whole of the precordium, not just the areas described. The areas mentioned above are useful for the description of clinical findings and drawing conclusions; otherwise auscultation should not be restricted to these areas. Auscultate whole of the ~recordium, either starting from the apex, movmg up along the left parasternal border to the pulmonary area and then to the AI area or • startmg from the A area and moving towards the 1 apex (Fig. 3.40).

• 1:ig · 3 ·4(): Dir , ·t · cc 1011 of auscul tation

•

Chapter 3-Cardiovascular System • •

•

•

Auscultate in supine position, at first with the diaphragm and then with the bell. Turn the patient to the left lateral position and auscultate at apex with the bell for middiastolic murmur of mitral stenosis. Ask the patient to sit up and lean forward, and auscultate the pulmonary and ~ areas with the diaphragm. Patient should hold his breath on inspiration for murmur of pulmona1y regurgitation and on expiration for murmur of aortic regurgitation. Before finishing auscultate bases of the lungs on the back for basal crepitations.

Auscultatory notation On phonocardiographic recording heart sounds appear as vertical blips, the height representing loudness and width duration. Murmurs resemble shading. Similar graphic notations are used to describe auscultatory findings. Interval between S 1 (first heart sound) and S2 (2 nd heart sound) is systole and interval between S2 and S1 is diastole (Fig. 3.42B). During auscultation note the following:

1. Heart sounds (first, second, third and fourth) 2.

Other sounds (opening snap, ejection systolic click, mid-systolic click, prosthetic valve sounds)

3.

Murmurs

~ricuspid valve lies between right atrium and nght ventricle and has three cusps. Aortic valve lies between left ventricle and aorta and has three cusps. Pulmonary valve lies between right ventricle and pulmonary artery and has three cusps. First and Second Heart Sounds The first heart sound is produced by closure of the mitral and tricuspid valves. It marks the beginning of systole. The mitral is the major component; the tricuspid component is comparatively quiet. Its maximum intensity is at the apex. The second heart sound is produced by closure of the aortic and pulmonary valves. It denotes the end of systole and the beginning of diastole. The pulmonary component is localized to the pulmonary area while aortic component is audible all over the precordium with maximum intensity at the A 1 area.

How to Differentiate Between First and Second Heart Sound? 1.

Palpate the carotid artery while auscultating (Fig. 3.41). The sound which comes just before the carotid pulsations is S 1 and the sound which comes after the carotid pulsations is S2• Similar relation exists with the apex beat (Fig. 3.42A).

4. Pericardia! rub Heart Sounds There are four valves in the heart. Their closure produces sound while opening is normally quiet. The valves between atria and ventricles are called atrioventricular valves; the valves between ventricles and major vessels are called semilunar valves.

Mitral valve lies between left atrium and left ventricle. It has two cusps (or leaflets); anterior and posterior.

49

Fig. 3.41: Palpation of carotid while auscultating

- ~

~

: ld~ =t~ b~ ~ 5~0 _ _ _ _ _- - - - : - -~ commen : out Its inten . . , - - - - - -- - - - - - - - -- - - and you shou s1iy apex on y. the to w ith reference Carotid pulse Carotid pulse Second heart sound. It is usually possib\ e to f. b h . find out the intensity o its ot components A

SI

S2

SI

•

Ifs ? is single and its intensity is loud at the ul~onary area whi le normal at the . aon1c P area, P 2 is loud.

•

If 52 is loud, both at the pulmonary area and aortic area, ~ is loud.

•

If 52 is of normal inten~ity at the pulmonary

S2

area and soft at the aortic area, ~ is soft.

B

Diastole

Systole SI

S2

Concentrate on S 1 while auscultating at I apex and tricuspid area. SI

Fig. 3.42: (A) Relationship of heart sounds w ith c:irotid pulsation (B) First (\ ) and second (S1 ) heart sounds; systolic and di astolic intervals

2. At normal heart rate the systolic interval is shorter than the diastolic interval. This difference can be recognized with e:,.,_rperience. The sound which comes at the beginning of the shorter interval (systole) is S 1 and the sound which comes at the end is S2 (Fig. 3.42B). This requires practice.

The sound which comes just before the carotid pulsations is S 1• The sound which comes after the carotid pulsations is S 2 . 3.

First and second heart sounds can also be recogn ized by their character; this requires lot of experience.

•

Soft P? is difficult to appreciate. Single S, of norma"'l intensity is an indirect evidenc~ of soft or inaudible P 2 •

•

If S2 is splitted, both components can be easily appreciated and their intensity can be commented upon .

Causes of abnormal intensity of heart sounds Soft both heart 1. sounds 2. Loud S I Soft SI

Note th e following two characteristi· cs o f h eart sounds:

Loud p 2

~

Soft p 2

~

Intensity

~Loud~

2. Splitting

Soft~ l11trusit)'

N orma l intensity of hea rt soun ds 1·s 1 earned w· 1 It 1 practi ce.

First heart sound . It is best audib]

1 apex e at tic

s1

Pericardia! effusion

3.

Emphysema Thick chest wall

1.

Mitra! stenosis

2.

Tachycardia

1.

Mitra! regurgitation

2.

Heart fai lure Rheumatic carditis

3. Variable intensity of

Characteristics of Heart Sounds

I.

Concentrate on S 2 while auscultating I aortic and pulmonary areas.

1. 2.

I

Atrial fibrillation Complete heart block

Pulmonary hypertension _ s1s Pulmonary valvular ste 110 Systemic hypertension Aortic stenosis Aortic regurgitation

~

Splitti 11,~ 111 First h 111111( . . • . eart sound: lts sphmng 1s unco and 111s·1gn1·ri1cant.

Chapter 3-Cardiovascular System

Second heart sound: Its splitting is very common and significant. Search for the splitting of S?at the pulmonary area beca use P? is audible only at that area. Splitting of S? i; of three types; usual splitting, fixed splitting and reverse sp litting. Usttal splitting: It means interval between ~ and P2 is more during inspiration than expiration (splitting is more prominent during inspiration and sound becomes single or splitting is narrower during expiration). it is explained below. Right sided cardiac output increases during inspiration and left sided cardiac output increases during expiration. Normally the aortic valve closes earlier than the pulmonary valve. During inspiration as negative intrathoracic pressure increases, venous return to the right atrium is increased which leads to increase in the right ventricular stroke volume. The right ventricle takes longer to empty itself, closure of the pulmonary valve is delayed and so is P2 .

Ca uses ef usual splitting ef S 2 1.

Normal in children and young adults. It is also called physiological splitting.

2.

Right bundle branch block

3.

Dilated right ventricle

4.

Pulmonary hypertension (split is narrow)

Fixed splitting: In atrial septa[ defect blood flows from the left atrium to the right atrium. The right sided stroke volume is increased three times normal and P 2 is delayed, resulting in wide splitting of S2 • As both atria are communicating with each other, the differential effect of respiration on stroke volume of two sides of the heart is lost and the interval between ~ and P remains constant during inspiration and expira~ion. This is called fixed splitting (Fig. 3.43). This is the most important sign of atrial septa! defect. Expiration

As lung expands during inspiration, blood containing capacity of pulmonary vasculature is increased· more blood is retained in the lungs, venous re,turn to the left atrium is decreased and so is the left ventricular stroke volume. The left ventricle empties itself in shorter time, closure of the aortic valve and ~ so produced are early (Fig. 3.43) . Hence during inspiration P2 is delayed and~ is early, resulting in splitting of S2 . During expiration reverse occurs. Venous return to the right atrium and the stroke volume of the right ventricle are decreased and P2 is early. More blood goes to the left atrium, stroke volume of the left ventricle is increased and ~ is delayed. As a result S? is , either single during expiration or th e split is-narrow (Fig. 3.43). An important point to be remembere? fr_om above di scussion is that during inspiration right sided cardiac output increases w~ile left sided cardiac output falls; durmg expiration reverse occurs.

51

51

I

Inspiration

Usual splitting

52

A2P2

51

A2P2

51

52

Fixed splitting

11

51

A2P2

II II

51

II

Reverse splitting

51

P2A2

fi g. 3.43: Splittin g of secon d heart souud

Reverse splitting: If left ventricular e~nptying is delayed to the extent that closure ot the :iorttc valve occurs after the closure of the pulmonary valve, the effect of resp ir:ition on sp litting of S2 is reversed , i.e. , it is more during expiration and

- - -~5?_ 2 ____________- - - -~ fourth Heart Sound · . Tl11·s 1s ca lled reverse Th . is a low pt·tc h e d sound a n d occurs· less during inspiration 1s . . . 1n lat c.,

splitting (Fig. 3.43). .., ..,

d. t le due to atnal contraction if ventri I e ias o . d d. c es are •ff or non complaint ue to 1sease (Fig st1 · 3-45)

Causes ef reverse spiitting of S2 I I.

Left bundle branch block

2.

Hypertrophic obstructive cardiomyopathy

3.

Severe aortic stenos1s

4.

Ri ght ve ntricular pacing

Sl

•

I

I

S2

S4

.

SI

Fig. 3.45 : Fourth heart sound

Splitting of the second heart sound Causes . Type of splitting Description Interval between ~ and p is 1. Children and young adults (physiological Usual .splitting 2 more during inspi~·ation and less during expiration. 2.

Fixed splitting

Reverse splitting

splitting) Dilated right ventricle

3.

Right bundle branch block

4.

Pulmonary stenosis if P2 is audible

5. Pulmonary hypertension (split is narrow) Split 1s wide and interval Atrial septal defect between ~ and P2 is the same during inspiration and expiration. Interval between ~ and P 7 1. is less during inspiration and 2. more during expiration. 3.

Left bundle branch block Hypertrophic obstructive cardiomyopathy Severe aortic stenosis

4. Right ventricular pacing Third Heart Sound Thi s is a low pitched sound and occurs in early di astole at the time of rapid ventricular filling (Fig. 3.44).

Causes effourth heart sound 1- Hypertension 2·

Ischemic heart disease

Note:

• SI

S2

S3

Fi g. 3.44: Third hea rt ~o und

f Ca11ses of third heart s01111d 1.

2. 3.

4.

C hil d ren ;m d h ea lthy yo un g adults Pregn an cy H ea rt fa ilure M itr:-1 1 rc£.!_1rgitati o n

Si

Bot h S and S are low pitched soun d·) .·111d 3 4 are more clearly audibl e with th e bell.

•

B h

ri,,hr Ot heart s?unds may origin ate fron~- \~•if or !~ft ve ntricl e . Le ft sid ed sound::. ,\IL (h 11 audible at < t I1e apex whil. e n.g Ilt s 1·dc-d so11 are be s t au d"bl 1 c at left para stcrna i lJO rdc:f•

Both s . le withet .i and S are best audtb t h e b 11 4 t Jc1' e ' at apex if left sided and a Parastern I b a order if right sided.

53

Chapter 3-Cardiovascular System

Gallop rhythm or triple rhythm: Presence of 3rct or 4 th heart sound (S_, or S) gives an auditory impress ion of the galloping of a horse and is called gallop rhythm or triple rhythm (three so unds).

Summation gallop: Both S3 and S may 4 be audible in the same patient. At slow heart rate both are appreciated separately. If heart rate increases, S3 and S4 come very close to each other and are inseparable. This is called summation gallop (Fig. 3.46).

Ej ec ti on Sys tolic Clicks The se are sharp systolic sounds produced due to th e opening of the abnormal aortic and pulmona1y valves and are heard soon after S (Fig. 3.48). The aortic click is best heard at the A 1 area and apex. It is not affected by respiration. The pulmonary click is best heard at the pulmona1y area and increases in intensity during expiration. If click is audible along with other signs of stenosis, it means stenosis is valvular rather than supra or subvalvular.

1

Presystolic gallop: It means S4 is present.

SI

Sl

S2

S3S4

Sl

ESC

S2

SI

Fig. 3.48: Ejection systolic click

Fig. 3.46: Summ ation gallop

Causes ef ejection systolic click Pericardia! Knock This is loud but distant diastolic sound audible in constrictive pericarditis due to abrupt halt to early diastolic filling of the ventricle. This can be described as distant )rd heart sound.

Aortic click

Pulmonary click

Other Sounds

1.

Aortic valvular stenosis

2.

Bicuspid aortic valve

3.

Pulmonary valvular stenosis

4.

Dilatation of pulmonary artery (idiopathic or due to pulmonary hypertension)

These include opening snap, ejection clicks and sounds of prosthetic valves.

Opening Snap In mitral stenosis a sharp high pitched sound is produced due to the opening of the mitral valve. It is audible soon after S 2 and maximum intensity is medial to the apex (Fig. 3.47) . Presence of opening snap means valve cusps are stenosed but mobile.

SI

S2

OS

I 1g. 3.47: O pening snap

SI

Mid-Systolic Click In mitral valve prolapse (a condition in which a cusp of mitral valve prolapses into the left atrium during systole) a click is produced in the mid systole which may be followed by a late systolic murmur (Fig. 3.49).

SI j=j ,.

MSC

S2

J.4 1) : Mi d- sys tulic cli l.' k

SI

1

Charac teristics of A Murmur =-=-=-=-=-=-=-=-=-=-=-=-.:-_:-_-_:-_:-_:-_:-_-_:-_:-_:-_:-_:-_:-_:-_:-_:-~~~~ - ~ - - -~5~4

ESC

SI

11I S2

OS S3

I

S4

I

If a murmur is audible, note characteristics:

Fig. 3.50: dded sounds: ejection systo lic click, op-cni ng snap, third and fo urth heart sounds

the follow· lf1g

.

SI

~

1.

Timing

2.

Intensity

3.

Site of maximum intensity

4.

Radiation

5. Character Pitch

Prosthetic Valve Sounds

6.

Prosthetic valves are of two major varieties:

7. Effect of respiration

Biological valves: These are of animal tissue

8.

and produce sounds similar to the normal heart sounds.

Timing

Mechanical valves: These valves produce sounds both at the time of closure and opening; there are four sounds rather than two. The inten sity of these sounds is loud and character is metallic and pitch is high . Mitra! valve produces metallic first heart sound and a sound like loud opening snap Aortic valve produces metallic second heart sound and a sound like loud ejection systolic click.

Effect of posture

For a beginner it will be sufficient if he can differentiate between a systolic murmur and a diastolic murmur. Palpate the carotid artery while auscultating. The murmur which comes with the carotid pulsation is systolic and the murmur which alternates with it is diastolic.

Systolic Murmurs There are two major types of systolic murmur.

Murmurs

Pansystolic murmur: It starts with S1 and goes

These are abnormal sounds and are of longer duration as compared to heart sounds. These are produced due to the turbulence of blood flow and o n e of three mechanisms is involved.

up to or beyond S2 (Fig. 3.51).

1.

va lve, e.g. , severe anemia or pregnancy. Such murmurs are also called functional or flow murmurs. 2.

3.

I I I II I II II II

Excessive flow of blood across a normal

Flow of normal amount of blood across a narrowed valve , e.g., mitral stenosis or aortic stenosis. Flow of blood in abnormal direction: a.

I allows a va lve Normally on ly I fl ow. If ·It is ab · ·d· um 1rcct1 o na norn1a < •

leakage

may occ ur, e.g., r1;e11ri itatio11 or aortir reg11rgitation.

niitrai

. . communication 1111 Wit 1 . tht: h c:1 rt. t: .g .. atnal septa/ dc~•rt 1 , . .J l , ' ( 11tnr11lar septa/ d1fi'rt or 0 11t ~idc tlic J1 .. . . l.llt, c.g , . pcrs1stc111 durtw arlt'rtns 11 s.

h. Abnormal

L

· '

SI

PSM

~ S2

SI

· murmur Fig· 3 __,~1-. p an systo 11c

Causes of pansystolic murmur 1. Mitra} regurgitation 2 · Tricuspid regurgitation 3· Ventricular septal d efect

.Ji,,hd1 E"e · .~ 1 ction systolic murmur: It scares ~ rht' · after th e. fiII--st 11eart sound :md en d ::,. L) L·tt>l"L ht' l •rwcc ll t . seco nd 11 , . l'.a1 t so und . There 1s a gap JL . • lt i~

. , . s1dL heart soui 1d .. d . !c!it" s an the murmur on c1c 11c 1 . . ... . . I1L' n11c . . . soft 1niti ·1II • ,111 r 111 max1111um 1s ' Y, 111tcns1ty and thc1 1 cIccrcascs (it is diamon d ::,·I1•·1pC'1 plionocardiography) (Fi g. 3.52).

Chapter 3-Cardiovascular System

55

Causes of murmurs Timing Finer timing Causes Systolic Pansystolic Mitra! regurgitation

SI

ESM

S2

1hcuspid regurgitation

Sl

Fig. 3.52: Ejection systolic murm ur

Causes of 1cm between affected and normal side is significant .

•

Forceful dorsiflexion of foot causes pain in the calf (Homan's sign). This test is usually avoided because a clot can get dislodged and lead to pulmonary embolism .

WRITING OUT ROUTINE EXAMINATIO N Examination of a normal person should be described as follow. If there are abnormalities these should be described at appropriate places. •

Pulse is 72/minute, regular, normal volume, normal character no radiofemoral delay, ' vessel wall not palpable.

•

BP 132/84

• )VP not raised •

Edema feet absent

Precordium

Inspection

Sl1 ape normal, no scar, no pulsations . "bi ovrr vtSI e the precordium.

Palpation

A pex beat palpable in S1h intercostal space 1ucd1:1I 1 to midclavicular line, of normal character. N.\ o th er sound palpable. No thrill. Left para 5rcni.t heave not palpabl e. A11sc11ftatio 11 Both h" ·11·t , . -11~irv. N(l '-• soun d s arc of norma 1 111cc ., • 1 . , . added so d un s, no murmur no basal crcp i·r::1' 0011· '

C HAPTER

Respiratory System The yield in the examination of respiratory system is variable. Diseases like asthma can be di agnosed with confidence on the basis of clini cal evaluation alone; on the other hand in tube rcu losis disease may be fairly advanced but clinical examination might still be normal. So, in add ition to detailed history and thorough physical examination, appropriate investigations are necessary to arrive at the correct diagnosis.

ANAT OMICAL CONSIDERATIONS Both lungs are divided into upper and lower lobes by the major fissure. Right upper lobe is further divided into upper and middle lobes by the minor fissure. So the right lung has three lobes and the left has two.

SURFACE ANATOMY 1. Bifurcation of Trachea: It correspo nd s

2.

with the sternal angle (also called angle of . b e tw ee n 4th and Louis)* in front and the d 1sc 51h thoracic vertebrae behind. · d rawn firom the 2'"1 Major Fissure: A lme thoracic spine to the 6th rib in the mammary . e represe nts the maJOr · fi1ssure · Upper lobe lm is mainly on the front and lower lobe on th e back.

3. Minor Fissure: A horizontal line drawn h from th e sternum at the level of 4' cos_tal ca rtil age laterally till it cuts th e line of niaJor · 1. fissure on th e fi1ssure, represe nts t I1e 1111110 · right sid e. 4- Base of Lung: On the ri ght SI"de it IS . JOilllll . . represented by a l111e g 6"' nb 111 the * I t .t \ th e junction u( 111 :i n 11 I, rtlllll . of s·t L·rni with body .. . I I ('. .. tltL" s t1pras lLllt ,1 t l C Sternum . M ovtll . f . . c.II c O ( tit..l)iration, and note any interval between them. Patients with pleural pain should not be asked to cough or take deep breath until pain is controlled. In such patient test vocal resonance first and if there is an area with abnormality, ask him to take one or two deep breath to assess breath sounds. When abnormal breath sounds are heard, map out the area by moving from normal to abnormal area.

Intensity of Breath Sounds Normal intensity is learned with experience. If intensity of breath sounds is diminished repeat auscultation after forceful cough; intensity of sounds will increase if it was diminished due to bronchial obstruction by secretions which are dislodged by cough. Causes of diminished breath sounds are: 1.

Pleural effusion

2.

Pneumothorax

3. Collapse with obstructed bronchus 4. Thickened pleura 5. Emphysema (reduction in intensity of breath sounds is generalized)

Character of Breath Sounds Vesicular Breathing: This is the character of normal breath sounds. It has the following characteri stics (Fig. 4.22) : 1. Inspiration is longer than expiration b~causc sounds arc audible throughout inspiration . . - I one tli · -d of expiration. b utduringonly m1t1a 1 1 •

Bronchial Breathing: It has following characteristics (Fig. 4.23): 1.

Expiration is as long and as loud as inspiration because sounds are audible throughout expiration.

2.

There is a definite pause between inspiration and expiration.

3.

Character of both inspiratory and expiratory sounds is blowing.

L __ Fig. 4.23: Bronchial breathing

(Breath sounds are produced by the passage of air through major airways and are originally bronchial in character. Their character is modified while being conducted through the lung tissue to the chest wall and becomes vesicular. If the intervening lung tissue is cut off and the sounds produced at major ai1ways are directly conveyed to the chest wall , their character remains bronchial.) Bronchial breathing is normally heard over the trachea and the upper part of mid line. Causes of bronchial breathing 1. Consolidation 2. Cavitation (may be a111p/l()rir rcsclllbling the sound produced by blowin g across the top of a bottle) 3. C olla sc v,1 ith patent 111ain bronchus

86 f high pitched Above mentioned causes arc O . I -d . Sometimcs . low p1tc 1e bronchial breathmg. . d . breathmg . .1s 11eai·d 111 · fibrosis an bronchial

bronchiectasis. · n 'and .tension In some cases of pleura 1 e fir,usto pneumothorax faint bronchial breathmg may be heard due to underlying compression collaps\ C ombination of consolidation and ~l~ura effusion may be difficult to diagnose chrncally. Percuss ion note will be stony dull, brea th sou nd s will be bronchial but of diminished intensity. Bronchovesicular Breathing: Inspiration is bronchial while e:x-piration is vesicular. It has no significance. Vesicular Breathing with Prolonged expiration (Fig. 4.24) : It is heard in chronic bro11c/1itis, e111physema and bronchial asthma.

and severe asth~ 1 . ic bronchitis Jnc11on ..._ . nch .ble both m msp11 at1on and expir . 1 a re au d 1 , ' . at1on •id asthma they are audible at the end · In 1111 . . of .. · only when patient 1s asked to expll atto 11 . . ope 11 t 11e m Oll th , take a deep 61 eath m and tlien . . c.ully as much as he can. In severe asth exrpuet' ' . . . . n1a the chest may be silent 1f _a1r entry 1s markedly reduced. A constant low p1tc_h ed ronchus (fixed ronc hus) is a feature of partial obstruction of a major bronchus, e.g., due to tumor or foreign body.

Stridor It is a sound resembling ronchus produced by partial obstruction of la,_ynx_and trachea. Its '.ntensity is louder in insp1rat10n (ronchus 1s more prominent during expiration) and decrease as one auscultates away from the center. Crepitations These are interrupted, crackling sounds produced by the following mechanisms:

Fig. 4.24: Vesicular breathing with prolonged e:'\.-µ irati on

Added Sounds

If added sounds are present, note their type, number and site where they are heard. You should repeat auscultation after forceful cough. It will help to differentiate between various added sounds if there is any doubt; ronchi or crepitations will alter while pleural rub will remain unchanged . Similarly, crepitations at apex after coughing may be the only sign of pulmonary tuberculosis.

Bubbling of the air through secretions in the bronchi and pulmonary cavities: These are heard throughout inspiration and change on coughing. Causes are bronchitis, bronchiectasis, resolving pneumonia, tuberculous cavity and lung abscess. These are heard over the affected part of the lung. Explosive reopening of thickened alveoli: These are heard at the end of inspiration and don't change on coughing. Causes are pulmona,1' edenit1 and fibrosing alveolitis. As closure of alveoli is more 1 1 l"k · e Y to occur at bases, such crepitattons 'art' more common there.

Causes of Crepitation s

Ronchi

TyPe of crepitations

Causes

Th ese arc continuous, musical, whistling sounds produced by passage of air through narrowed airways. These are audible all over the chest.

Pan inspiratory

Bronchitis Bronchiectasis

Causes of ronrhi

Resolving pneumonia

1. 2. 3.

Tuberculous cavity

Bron chi al asthma C hroni c bronchiti s Em phy sem a

Lung abscess End inspiratory

Pul111011ary cdc111a Fibrosing alveoliris

---

- - - - --:-==-- - - - - - - - - -- - - - -- - -~C~h~a£p~te::_r~4~ R~e~s£p~ir~at~o~rI_ y~Srys~t~em ~ _J8~7~ - -

Pleura l Rub This is a superficial, scratchy, rough sound (similar to pericardia! rub) and is produced by rubbing of inflamed pleural surfaces. It does not change with coughing. It is audible at the end of inspiration and just after the beginning of e>..-p iration. It may be audible only on deep breathing. It disappears with the development of effusion but may persist above the effusion.

Whispering Pectoriloquy Ak h s t e patient to whisper words like one one on e. N orma 11 y these are not clearly appreciated ' ' on. . auscu ]cation . If individual syllables are ~1st1~ctly appreciated, whispering pectoriloquy 1s said to be present.

Causes of abnormal vocal resonance and

whispering pectoriloquy 1. Increased vocal resonance and whispering

Table Differential diagnosis of pleural rub and crepitations Pleural rub

Crepitations

It is audible at the end of insp iration and just after the beginning of e>..-p iration It increases in intensity on pressing the stethoscope It remains unchanged on coughing

These are audible only during inspiration

pectoriloquy: Same as those of increased vocal fremitus and bronchial breathing (page 81) 2.

Decreased vocal resonance: Same as those of decreased vocal fremitus and decreased intensity of breath sounds (page 81)

These are not affected

Forced Expiratory Time (FET) These usually change on coughing

Vocal Resonance It is similar to vocal fremitus but is heard on auscultation. Ask the patient to repeat words like one, one, one or equivalent, and auscultate the chest. A resonant sound is heard and is called vocal resonance. Compare it at corresponding sites on both sides . Vocal resonance may be normal, decreased or increased. Normal vocal resonance conveys the impression as ifit is being produced just at the chest piece of the stethoscope. If it seems that the sound is being produced nearer the ear than at the chest piece, vocal resonance is increased.

Bronchophony: Sometimes vocal resonance increased to the extent that it coveys the impression of being produced near the ear piece of th e stethoscope. It is called bronchophony.

15

.Aegophony: Sometimes a nasal or blea ting quality is added to th e sou nd of vocal reso nance. It is called aegophony. It usually occurs above th e level of a large pleural effusion.

Place the chest piece of stethoscope over the trachea. Ask the patient to take full deep inspiration and then expire fully at maximum speed. Note the time taken by expiration. Normally it is less than 4 seconds. It is prolonged in chronic bronchitis, emphysema and bronchial asthma.

Coin Test This test is sometimes helpful in confirming the presence of tension pneumothorax. Take help of another person. Ask him to place a coin on the posterior chest wall of the patient and tap it with a second coin while you auscultate on front. Normally a dull thud is heard. If a ringing metallic sound is heard, test is positive.

Succussion Splash If the chest of a patient with hydropneumothora.,x is shaken, a splashing sound is hea rd. It should not be confused with gastric succussion splas h (page 111 ).

- --

r

I

ex

ex

SIGNSOFVARIOUSRESPIRATORYCONDITIO NS

Pathologic al condition • Consolidation

-

I

Cavita tion

Shape and defonnity Movements of Mediastinal chestwall of the chest displacement May be reduced None N urm:il on affected side

Percussion Breath sounds note Impaired or Bronchi al dull

N orma l

Impaired

CoHapse wi th patent Loca l fl attening maybe present bronchus

M aybe reducedon affected side M aybe reduced on affected side

Collapse with Local fl attening obs tructed bronchus may be present

Maybe reduced on affectedside

Towards lesion Impaired or Diminished dull or abse nt

Maybe reduced on affected side

Towards lesion Impaired

--

Fibrosis, bronchiec tasis

Local flattening may be present

N one

Bronchial

Towards lesion Impaired or Bronchial dull

Vocal Added sounds resonance In creased, C repitati ons whispering pectoriloquy, Increased , Coarse whispering crepitations pectoriloquy Increased , N one whispering pectoriloquy N one Reduced

M ay be bronchial

M aybe Increased Reduced or absent

\

I

\ I

Coarse crepitations

\

1

Pleural effusion

'Local bulgingmay bepresent

Reduced or absenton affected side Reducedor absent

Towards opposite side

Stony dull

Diminish ed or absent

Towards opposite side

Hyperresonant

Diminished or absent

Diminished all over

None

Normal

Chronic obstructive Barrel shaped chest Diminished all airway disease over

None

Normal or hyperresonant

Vesicular with Normal prolonged expiration Diminish ed Normal or vesicular with reduced prolo nged expirati o n

None

N o rm.a l

Pneumo thorax I

Bronchial asthma

Local bulging may be present Normal, maybe barrel shaped

'

-

\lnterstitia\ \ung

N o rm a\

disease

Diminish e d all over

Ve s ic ul a r

\

Pleura\rub above the effusion in some cases Reduced or None absent

N orm a l

Expiratory ronchi

Ron chi (may be bo th inspiratory and expirato ry) E11d inspirato ,y

-

e r e p i t .1 tio , IS, I IO t

\

.-, fTc.: crccl h y c 11.~ l,i11.t..:· I

}

, ., - ,..----------~~~~~===~~=~-----

Chapter 4-Respiratory System

89

SUMMARY OF EXAMINATION ~ ~E~C~T~IO~N~ - ~ R~e: sp~i~ra~t~o ~ ry~1~a-:te:--- - ---== ~~ ~ ~~ - - - - - - - ----1 ~

Type of respiration

J

Abdomino-thoracic or thoraco-abdominal Acidotic breathing Cheyne-Stokes breathing

Shape of the chest

Normal Barrel shaped

Deformity

Pectus carinatum (pigeon chest) Pectus excavatum (funnel chest) Harrison's sulcus Thoracic kyphoscoliosis Local bulging or flattening of the chest

Prominent veins, pulsations, scar Chest movements

PALPATION

Reduced movements Indrawing of intercostal spaces and supraclavicular fossa Paradoxical movements Use of extra respiratory muscles Pursing of lips

Position of trachea and apex beat Movements of chest Expansion of chest Vocal fremitus Tenderness, crepitus

______ _ _j ~P~al~p'.:a~b~le~s~o~u~n~d~s- - - - - - t - - -- - - - - - - - - -1

PERCUSSION

Upper border of liver Comparison of percussion note on both sides

--i-;:::~-;--------Intensity

_ _ _ _ _J 2T~id~a~l_!p~e: r::c~u:ss~i~o~n_ _ _ _ - - AUSCULTATION Breath sounds

Add ed sound s

Voca l re so nan ce Whi spe rin g Pccto ril oqu y

. ,pir:iwry ti111 c Force d ex '

C haracter Ronchi C repitations Plcur:il rub

90 WRITING OUT ROU TINE EXAMINAT ION Examination of a normal person shoul~ . be described as follows. If there are abnormahues , these should be described at appropriate places.

structive lung diseases (chron ~ 1 . . . onc'7;1;5 In o b ,sema asthm.a) rate at which air is exh , e/11 Pl1 } ' . . a1ed ·

decreased throughout e:>-...rpiration. Total len Is_ · · · · d FEV 1 • gtho1 exp iration IS mc1 ea~e . is ma1•kedly reduc d FEV 1/ FVC% IS decreased . In rest . _ed a1l . rtctiv lung diseases if,brosing alveolitis, ank 1 . e spondylitis) FEV and FVC both are redute:Uig same proportion and FEV 1/FVC% is normal In 1

Inspec tion Respiration rate is 16 per min. Respiration is abdomino-tho racic. Shape of the chest is normal. No deformity, scar, prominent veins or pulsations visible. Apex beat is visible close to the nipple. Chest is moving equally on both sides with respiration. Palpation Trachea is central. Apex beat is palpable in 511, intercostal space medial to the midclavicular line; it is of norm al character. No tenderness or crepitus demonstrated . Movements of the chest are equal on both sides. fa-...7Jansion of the chest is 5 cm. Vocal fremitus is equal on both sides. No sounds are palpable. Percussion Upper border of the liver is in 5th intercostal space. Percussion note is resonant and equal on both sides.

Auscultation ~reatl~ sounds are vesicular and of normal mtens1ty. !here are no added sounds. Vocal resonance 1s equal on both sides.

There are different types of spiro b II . . ·1 . meters ut they a give sum ar mformation. Ask the . take in as deep a breath as possible and t:at1ent to as hard and as fast as possible 'T: I en exhale . I . iota amou f alf expe led is called Fore d v· nt o FVC) Th e ttal Capa . ( . e volume of air ex ell . city 111 second is called Forced E . p ed first in one second (FEV1) R ~ptrfatory Volu111 . e · at10 o F£v1 d in percentage (FEVlfFVco;.) . an FVc . II . . o is a useful .111 d N 01 ma y 1t 1s b'lTater than 7oo1i M .d _ ex. Flow Rate (MEFR) which i . ob. . 1 -Expiratory . so tamed fr10 sa me record 1s a better pa. m the 1ameter fo.1 . .. o bstJ uct1 011 compa red with PEFR ( an way sec below). •

•

This is measured by a device called peak fl . . ow m eter. A simple version m common use at horn and on the bedside is mini peak flow rnet er.e Ask the patient to blow forcefully into it after a full inspiration and note the reading. Calculate average of three readings. Normal value is greater than 400 L/min. It is reduced in obstructive ai1way disease. This is very useful for bedside and at home assessment of airway obstruction and response to treatment.

Aspiration of Pleural Fluid Diagnostic aspiration is done when the cause of effusion is not known. A sterile needle is inserted P0st eriorly at the site of ma.,'(imum dullness. Ab~ut ~O ml of fluid is aspirated and sent for e st1 mat 10n of proteins and stwar number and f t:, ' type 0 _ cells, staining, culture and cytology. Large qu~nti~ has to be drained by slow continuous asp1rat1on · · . . throuo-h o a " g1vmg set" 1·r pIeuraI e £ifusion 1s co n t 11··b utmg · . to respiratory distress.

Causes of pleural effusion A. Exudate (more t h an 3 grams proteins per di)

Lung Function Tests Spirometry

•

Peak Expiratory Flow R ate (PEFR)

l.

Tuberculosis

2.

Malignancy

3·

Po 5t-pneumonic

4·

Pulmonary infarction

S.

Connective tissue disorders (SLf. rheumatoid arthritis) B. Transudate (I ess than 3 grams prate ins per di) C

1.

CongeS t ive cardiac failure 2· Hypoprot · · including ncp I1rotiC e mem1a

0

3.

~

syndrome I Meig's d syn rome (can be exu dative ,

o)

~_J9~1_ _ _ ys~te~m y~S:r to~rx_ ~e::s~p~ir~a~ - ~ - --=~- -- - - - - - - - - - - - - -~ C~h~a~p~te:_i:rj4~ R -----

Respiratory Failure

Type II Respiratory Failure

Respiratory failure is said to be presen t if either 1 8 kP (60 mmHg) or PaC02 is . 1 a PaO 2 1s ess t 1an more than 6.5 kPa (50 mmHg) . It is of two types. Type I Respiratory Failure

Pa02 is reduced and PaC02 is elevated.

Causes 1.

Chronic bronchitis

Pa02 is reduced but PaC02 is normal or low. 2. Emphysema

Causes 1.

Bronchial asthma

3.

Respiratory paralysis

2.

Pneumonia

4.

Severe kyphoscoliosis

3.

Pu lmonary edema

5.

Depression of respiratory center, particularly by narcotics and sedative drugs

6.

Acute severe bronchial asthma (late stage)

4. Pu lmonary embolism 5. Allergic and fibrosing alveolitis

DIFFERENTIA L DIAGNOSIS OF PLEURAL FLUID Condition

Colorof fluid

Cells Proteins concentration

Tuberculosis

It is straw

>3 G/dl

Lymphocytes

colored.

It may be hemorrhagic.

Other features AFB may be isolated from fluid on ZN staining or culture DNA may be detected.

"

"

RBCs

Malignant cells may be seen on cytology.

I

It is usually hemorrhagic.

! Post-

It is straw

"

"

Mainly polys

It is sterile on culture.

"

"

RBCs

Diagnosis is made on the basis of other features of the disease.

"

"

Mainly lymphocytes

"

"

"

..'-pression (patient may 1 Pam of p · ) . present TI . . ~111 • rebound tenderness 1s 11 · s mdicates peritonitis.* Mass: If a ma . features: ss is palpable, note the following

B

Fig. _s_.s: Sequence of palpation of abdo left iliac fossa to right hyp I d . men (A) from ·1 · oc 10n num (B) c. 1 1ac fossa to left hypocl10n d num . irom right

• •

1.

Site

2. Size 3 - Shape

To gain patient's confidence .

4·

To assess the tone of h t e abd 0 · muse Ies and to detect guard.mg · ·d·mmal tenderness. Guarding • . ' ngi or Is 1ocahzed ·1ty . produced by reflex c . ngidity . ontract1on 0 f abdominal muscles overl in . the y g an mflamed

*-"""'.s:-:. ----

Consistenc ** (

Y

. cystic, soft, firm, hard)

•gns of · movements f h peritonitis: Absent respirator)' O tenderness bt e abdominal wall rigidity guarding, ' ' I sounds (if pere• ou. ~ d tenderness 'and absent bowe ** ~onsistennton1t1s 1.~ ge_neralized). soft Uelly like) ~~Cy~t,c (hke water filled balloon), ver/ ' soJt (hke re I axed muscle),_fir111 (like u·p

I

Chapter S-Alimentary and Genito-Urinary System 1O1 mesentery are mobile; retroperitoneal masses, e.g., pancreas and masses attached to the anterior or posterior abdominal wall are not mobile)

A

12. Upper and lower limits of the mass (upper limits of liver, spleen and gall bladder and lower limits of urinary bladder and uterus are not reachable) 13. Bimanually palpable or not (kidneys are bimanually palpable) In order to differentiate between intra-abdominal and extra abdominal mass, ask the patient to raise his head against resistance. As abdominal muscles contract, an intra-abdominal mass will become less conspicuous, a mass in the muscle wall will not change while subcutaneous mass will become more prominent. Following masses other than the vtscera discussed later could be palpable.

B

Sigmoid colon: It lies in the left iliac fossa. It may be palpable as a tubular structure normally, as a tender mass in diverticulitis and as a hard ill-defined mass in carcinoma sigmoid.

Mass in right iliac fossa: A normal cecum

Fig. 5.6: Palpation of abdomen (A) correct method; hand is held flat relaxed and molded to the abdominal wall (B) incorrect method; hand is rigid and mostly not in contact with the abdominal wall

5. Surface (smooth, irregular, nodular) 6. Edge 7. Tenderness

8- Pulsatile or not 9. Bruit lO. Movement with respiration (liver, spleen,

th kidney and gall bladder move wi respiration) l 1. Mobility (masses originating from small entum and l · transverse co on, om Intestine, s of a body d b. 0 1 icep. t 1e nose), hard (like contracte builder}, stony or bony hard (stone or bone hke).

f

is sometimes palpable in the right iliac fossa as a soft ill-defined mass. Other masses at this site may be due to appendicular mass, iliocecal tuberculosis, carcinoma cecum or ameboma. In a female, masses related to fallopian tubes and ovaries may be palpable in both iliac fossae.

Hard feces: In a constipated patient fecal masses may be palpable. These are identified by the observation that finger pressure causes indentation of the lump. Abdominal aorta: It is palpated by pressing deeply the extended fingers of both hands, held side by side, above and to the left of the umbilicus (Fig. 5.7). In aneurysm of the aorta expansile nature of the pulsations can be determined (page 98). Gastric mass: In congenital pyloric_stcn~sis a tumor like mass is palpable in the ep1gastnum. In adults a gastric mass may be due to carcinoma stomach.

- - -- -~

102 . ph no d es .. Para-aortic Abdomma 1 1ym . ·ea between lpablc 111 t 11c a1 lymp h no d cs arc pa _r

eme1·gcs· on th e o rs:1 su1 , . uliq11c mu sc le. . . ·I , o N ,. Its 11uclc 11s ltL'S 111 t ll The Abducent erve . . .. . , . /at ,ra / rert/lS 1111 ts l k . It s11ppI rcs < pons. . t1'or1s· W h L· 11 \ \'L' 11 \ Ll\T , Connec · I Internuc car .· •I t or k fr. buth eyes , !I s- IIIJ. duv.rtl. r1~ I eye I1 •1 ·

138 eye move together. These are ea 11 ed co niugate ~ . l movements and are coordinated by the Media Longitudinal Bundle (MLB) which conne~ts nuclei of Jrd, 4111 and 6111 cranial nerves with each other. Conjugate eye movements are als~ controlled by centers in the frontal lobe an brain stem.

Examination At first neurological examination of the eye will be discussed and then examination of individual nerve.

Examination of the eye Palpebral fissure: Ask the patient to look straight and compare two sides to look for drooping of eyelid (ptosis).

Ocular movements: Stabilize the head of the patient with one hand. Ask him to focus at your finger held at a distance of two feet and follow it with his eyes. Ask the patient to report double vision (diplopia) if it occurs. Move the finger towards his right. In this way lateral rectus of his right eye and medial rectus of his left eye are tested. Move the finger upwards; superior rectus of the right eye and inferior oblique of the left eye are tested. Now move your finger downwards; inferior rectus of the right eye and superior oblique of the left eye are tested. Move the finger towards left and repeat up and down movements. In this way all the extraocular muscles are tested individually (Fig. 6.23). If patient reports diplopia note the direction in which images are maximally separated. It usually occurs in the direction of action of paretic muscle.

The Oculomotor Nerve Look for ptosis. Stabilize the patient's head with one hand. Ask him to look straight at your finger held at a distance of two feet and fo~low it. Move your finger medially (to test me~1al rectus) and then upwards (to test inferior oblique). Now move the superior fimger laterally and then upwards .(to£ test . rectus) and downwards (to test m enor rectus). Note any abnormality of the eye move~ent~. Ask the patient if he sees double; note the direction of movement in which diplopia occurs.

Keep your finger at a distance of two feet and stabilize the patient's head with other hand so that he cannot move his head while following your finger. Pupil: Look for size of the pupil and reaction to the light and accommodation.

Light Reflex: Its afferent path is through the 2nd nerve and efferent path is through the Yd nerve. Shine bright light into the eye from the side while patient looks straight focusing a distant object to avoid accommodation response. A hand should be placed over the nose to prevent the light from entering the opposite eye. Normal response is brisk contraction of the pupil followed by slight relaxation. This response occurs on the same side (direct light reflex) as well as on the opposite side (consensual light reflex). Both eyes should ~e tested separately and both eyes should be mspected each time to see direct and consensual response (Fig. 6.24). Differentiation of lesion of 2nd rd and 3 nerve are discussed on page 141.

Pupil: Note size, shape, and test light and accommodation reflexes.

Size: Compare the two sides and note whether pupils are of normal size, dilated or constricted.

Shape: Note whether it is regular or irregular. Light Reflex: Check both direct and consensual light reflex (page 138). Accommodation Reflex: (page 139).

Nystagmus: (page 141). Fig. 6.24: Eliciting light reflex

Chapter 6

Nervous System 139

mmodation Reflex: Ask the patient to look

~

Causes of 3,d Nerve Palsy

at a distant object and then look at his nose or at your finger held close to his nose. There is convergence of eyes and constriction of pupil.

1.

2. Aneurysm of the posterior communicating artery

The Trochlcar N e rve Ask the patient to follow your finger medially and then downwards (to test superior oblique) .

The Abducen t Nerve Ask the patient to follow your finger laterally (to

3. Midbrain lesion (there is hemiplegia on the opposite side, it is called Weber syndrome) 4.

rest lateral rectus).

In addition to the causes of 3 rd , 4th and 6th nerve paralysis discussed below, ocular movements are also weak or absent in myasthenia gravis (pupils are normal), ocular myopathy and Wernicke's enceplialopathy*. The eye doesn't move in the direction of action of paralyzed muscle and patient sees double when asked to look in that direction.

Third Cra nial Nerve Paraly sis

•

Cavernous sinus thrombosis (4 th and 6th nerves are also involved)**

Fourth Cranial Nerve Paralysis

Inter J ·eta tion

•

Diabetes mellitus (movements are painful and pupil is not affected)

There is ptosis due to paralysis of levator palpebrae superiors. Superior, inferior and medial recti and inferior oblique muscles are paralyzed. The eye ball cannot move medially a nd upwa rd s, and is deviated laterally and slightly downwards due to unopposed action of lateral rectus and superior oblique. Pupil is dilated and fixed. Light and

•

Superior oblique is paralyzed (Fig. 6.26).

•

Isolated lesion is rare.

Fig. 6.26: Left 4th nerve palsy

Sixth Cranial Nerve Paralysis •

Lateral rectus is paralyzed and eye ball 1s deviated medially (Fig. 6.27).

accom modation reflexes are absent (5 .25).

Fig. 6.27: Left 6th nerve palsy

~~ ~

•

(s__ . • Fig. 6.25 : Left 3rd nerve pa l~y

Because of its long intracranial _route , it . is 1 involved in rai sed mtrac rarna l . d is a false · common y pressure of any ettology an localizing sign. Iv c d. Jth . if 6tl' nerve 1.s 111vo .· . . , ·. . . In pontme 1es10 11 , ff- cted •·md there is he1111pk g1.1 o 11 I . IS a so a C th e oppos ite side.

*

. . due to ac ute Wcrnicke's encephalopathy i s nerves arc I .

d . efi cicncy of vitamin B 1; All the t ,rce irivolvcd alongwith enceph alopa t by.

** T hird. 4,11 , 6'" cranial nnw s rnd up hth~dmic ~i-visi~n

·,s·s tlirotwh the c 1vcrnou s 111us. .. , nr-" . I 11c1vc :::, . ofS'" cr:1111a

140 Internuclear Ophthalmoplegia •

•

When patient is asked to move the eye laterally, there is nystagmus of that eye (this is called ataxic nystagmus) and the opposite eye cannot move medially. Lesion is in the medial longitudinal bundle on the side of weakness of adduction (5.28).

• Bilateral internuclear ophthalmoplegia is characteristic of multiple sclerosis. 3rd nerve nucleus (Medial rectus)

MID-BRAIN

I

I

MLB --,-►~ I

Pupil Size Normal size of the pupil varies from 3 mm to 5 mm (Fig. 6.30A) . It may be dilated (>S mm) (Fig. 6.30B) or constricted ( ...1:ension of hip.

Reflexes

Fig;. 6.G6: Testing adductors of thigh

Abductors of Thigh Place your right hand on lateral side of th e leg. Place the patient's legs together and ask him to '>1.:paratc them against resistance (Fig. 6. 7 ).

These are dependent on the reflex arc which consists of an afferent limb and an efferent . 6 . The afferent ( ensory) limb transmw . . I1111 the impulses generated by the ·timuLltlon ut (or ncurnn . ~ recep tol·s to the communicating .cl in turn sends l1111ulus to neurons ) Wl 11 1 the effector organ (e.g., mu ·cle) thrnugh the efferent (motor) limb (Fig. (i.68). Whole r~lkx arc sho uld be illt,ICt for the reflex to be elic1~cd. Each reflex is c,11Tied out by one or two spmal

162 segments which is called root value of that refl ex; it should be remembered. Reflexes are of two types: deep reflexes - also called tendon j erks and superficial reflexes.

Fig. 6.68: Reflex arc (1) receptor (2) affe rent (sensory) limb (3) com m unicating neuron (4) anterior horn cell (5) efferent (motor) limb (6) effector organ (muscle)

Reflex

Root value

Ankle jerk

S1, 2

Knee jerk

L3,4

Biceps jerk

CS, 6

Brachioradialis jerk

CS, 6

Triceps jerk

C6, 7

Plantar reflex

S1

Abdominal reflexes

T8-T12

Cremasteric reflex

Ll, 2

Anal reflex

S3,4

Conjunctival and corneal reflexes

V, VII cranial nerves

Observe the following precautions while eliciting the tendon j erks: • Ask the patient to relax and be comfortab] e. •

The muscle being tested should be visib] e . . and look for its contraction rather than movement of the limb.

•

Hold the flexible shaft of the hammer frorn its end and let the heavy end of the hammer fall on the tendon to be tested.

•

Strike the tendon, not the muscle, because m echanical stimulation of the muscle belly produces contraction of the muscle that is not dependent on the reflex arc.

•

Compare each jerk with its fellow on the opposite side. If reflex is absent, elicit it again after reinforcement*. For reflexes oflower limb ask the patient to clench the hands or hook the fingers of both hands together and then pull them away from each other without disengaging (Fig. 6.69). For reflexes of upper limb, ask the patient to clench the teeth. This phenomenon of reinforcement only lasts for less than a second; therefore, ask the patient to perform appropriate maneuver when you are about to strike the tendon.

•

There ~re more than one methods of eliciting tendon Jerks. In order to avoid confusion we will desc~ibe only one method that we consider easy, and is practised by the majority of physicians.

Deep Reflexes (TendonJerks) These are: 1.

Ankle jerk

2.

Knee jerk

3.

Biceps jerk

4.

Triceps jerk

5.

Brachioradialis jerk

*remote Reflexes are increas d 111 . fi ' e amplitude when

l muse es rom those b · d forcefully. This is call ei?g tested are contracte ' ed remforcement.

Chapter 6- Nervous System

J 63

------Fig. 6.70: Eliciting bi ceps j erk

Fig. 6-69: Reinfo rcem ent phenomenon

Biceps Jerk (CS, 6)

Flex the elbow at right angle and place the forearm in a semipronated position. Place the . d ex finger of your left hand over thumb or m th e tendon of the biceps in the cubital fossa and st · o f tI1e · h t h e )iammer. See contraction b rike it wit iccps (Fig. 6.70). Triceps Jerk (C6, 7) , abd omen, . c Place t11e 1orear111 on the patients elbow being Ocxed at right angle. trike the ,, · tendo 11 o f t hc triceps above the olecranon . Scc · o f the triceps (Fig. 6.71 ). contra ction

Fig. 6.71 : Eliciting tri ceps j erk

Brachioradialis Jerk (CS, 6)

Thi is al o called supinatorjerk. Flex the forc:mn at elbow and place it in ·cmipro11.1tcd µo:ition . Bend the hand lightly tow:1rds ulnar ·idc. trike the tendon of the brachioradiali ·. proximal to the styloid pro css of the radiu -. • cc ·ontracti n of the bracl1ioradialis (Fig. 6.7-).

164

Fig. 6.72: E liciting brachioradi alis jerk

Fig. 6. 73 : Eliciting ankle j erk

Inversion of reflexes

Knee Jerk (L3, 4)

If a tendon jerk being elicited is absent/ diminished but there is contraction of muscles innervated from an adjoining spinal segment, this is called inversion of that reflex. It indicates combined spinal cord and root pathology and has a precise localizing value.

Patient should lie supine. Flex the knee and support it with your left hand. Feel for the tendon of the quadriceps and strike it between the patella and tibial tuberosity with the hammer. See contraction of the quadriceps (Fig. 6.74).

Inversion of the biceps and brachioradialis jerk: When biceps or brachioradialis jerk is elicited , it is absent/diminished but there is flexion of the fingers. Lesion is at the CS spinal segme nt. Inversion of one or both of these jerks h as the same significance. If flexion of fingers occurs and these jerks are normal/brisk, this is a feature of hyperreflexia and should not be confused with inversion.

Inversion of triceps jerk: When triceps jerk is elicited, it is absent but there is contraction of biceps. Lesion is at the C7 spinal segment. This is less common.

Crossed reflex induction: It means elicitation of a jerk produces reflex contraction of muscles on the contra latera l ide, e.g. elicitation ofknee jerk on one side may produce reflex adduction on thc opposite side. This is a sign of spinal cord lesion.

Fig. 6.74: Eliciting knee j erk

Clonus · 1untary, osc1llatory . mvo mu cu !1r ' contraction and relaxation invoked by a uddcn stretch of the muscle.

This

is

Ankle- Jnk (Sl, 2)

Patient c;hould lie supme. Flex the leg c; li ghtly an d place it in an externa ll y rotated po ·ition. Place your left hand on so le o( the foot and dorsiflcx it· strike the Achilles tendon w ith th e ltarn 111 1.:r. ' c~ the contraction of the ca lf muscles ( ig. 6.73).

Ankle Clonus Flex th e kn d . . h d cc an supp rt tt with the left an · GI rasp th c forcpart of the foot with the right 1a11d, dor ifl , , · h 1 . . ex tt suddenly 2 - 3 times and t et n1a1nta1n the d . 'l . . d r, . or It excd po ition by suc;tainc Pc surconthc 0 [ , I ~ . .,-re c. t clonu 1s present, chctc '1

reaular oscillations of the foot due to contraction relaxation of the calf mu scles (Fig. 6.75).

d

an

Chapter 6-Nervous System all the four limb

.

.

165

.

s ai e symmetncally mcreased (b n.s k), it is difficult d •d d u e to UMN I · to ec1 e whether they are

esion or not, beca use they are . 1 aDso _s~en 111 anxiety, thyro toxicos is and tetanus. ec1s1o n , then de d , pen s upon pl anta r res ponse (page 165).

Diminished

te n don Jer · ks: Reflexes are diminished if there is LMN d amage, as .m neuropathy, motor neuron disease, poliomyelitis and tabes dorsa/is . Reflexes are absent when sensory part of the reflex arc is affected o r there is complete paralysis of relevant muscles. Reflexes are usually normal in myopathies. fig. 6.75: Eliciting ankle clo1rns

Delayed

relaxation:

Patellar Clonus

Pendular jerk: (page 180)

In hypothyroidism relaxation time of the reflexes is increased. This is best seen in the ankle jerk.

fa1end the knee and grasp the patella between the thum b and index finger. Push it sharply towards the foot 2 - 3 times and then maintain the position. Regular movements of the patella occur if clonus is present.

Afew beats of clonus may be elicited in a nervous patient. This is called ill-sustained clonus and has no significance. Sustained clonus - the clonus that continues as long as stretch is applied - i~ a sign ofUMN lesion and is associated with bnsk reflexes (Fig. 6.76) .

Don't declare a reflex to be absent before eliciting it with reinforcement. Superficial Reflexes These are:

1.

Plantar reflex

2.

Abdominal reflexes

3.

Cremasteric reflex

4.

Anal reflex

5.

Conjunctiva! and corneal refl exes (page 144)

Plantar Reflex (S1) The patient should lie supine with legs ex1:ended. Grasp the ankle with left hand. Sc~atch the outer e d ge o f th e sole of the foot w ith some . 1·k a key sta rting from the heel blunt o b~ect I e ' . . cowards the littl e toe and then mcd1ally aero s . I Stop as soon as fir t movement th e metata1sa s. ' . . . , , .. . . It i a noc 1ccpt1vc 1efle'X,llld of the big toe occu1 s. , . stimulus must be painful, but irtjury to th, toot

lntcrprcta tion of Tendon Jerks

Ren cxe .

.

.

may be normal, m crcase

d or dimini shed .

In

. k . These arc a creased (brisk) tendon Jer 5 • · \t . 1 "fprcscnt Ill gn of UMN lesion, particular Y 1 . f 0

o d If rcncxcs nc limb or one half of th e bo Y·

. should be avoided. , · . plannr (k ion ol the ~rc,tt Norm al respon e , , , . . ,. .tl1 (le ·ion ,md ,tdduct1lHI l)I till' L)thc1 l toe a I011gw , · . "- 77) T l11-; i ,tlsu ·.tlkd downgomg lOCS (F- 1g . o. . . ., .

plantar or ll ('.~c1li11c Hci/,111.&1

''1.~11.

166 Oppenheim's si~n: E>ctensor plantar response is elicited by rubbm g over the crest of the tibia.

Gorden's reflex: Extensor plantar response is elicited by pinching the Achilles tendon. Both these signs are present when corticospinal lesion is widespread and severe .

Hoffman's sign: Hold terminal phalanx of patient's middle finger between your thumb and index finger. Flex it at terminal interphalangeal joint, and then flick it into extension with your thumb. If sign is positive, there is quick flexion of the patient's thumb. It is a sign of hyperreflexia; if unilaterally positive, it strongly suggests UMN lesion. It should not be confused with Homan sign seen in deep venous thrombosis (page 72). Finger flexionjerk: Place tips of your middle Fig. 6.77: Eliciting plantar reflex

If there is extension (dorsiflexion) of the great toe (usually accompanied by fanning of the other toes) , this is called upgoing plantar, extensor plantar or positive Babinski's sign. Sometimes extensor plantar response is accompanied by reflex flexion of the ankle, knee and hip joints; this is called withdrawal response. Its significance is the same as that of upgoing plantar alone. If movement of the big toe is not clear it is recorded as equivocal. Interpretation Upgoing plantar is the most significant sign of UMN lesion. There are other causes as well. In . UMN lesion upgoing plantar may be umlateral or bilateral, depending upon the site oflesion. In other situations it is always bilatera.1

and index fingers across the palmar surface of the proximal phalanges of the patient. Then lightly tap your own fingers. A slight flexion of the patient's fingers is normal but a brisk contraction suggests hyperreflexia.

Rossolimo's sign: Flick the distal phalanges of the toes into extension with your fingers and then allow them to fall back into normal pos~tion. A positive response is brisk plantar flexion ~f the great toe. This is a sign of pathological hyperreflexia. It is counterpart of the Hoffman's sign in the lower limb. It is particularly helpful when plantar response cannot be obtained because of paralysis of the extensor hallucis longus. Absent plantar response Sometimes n o P1antar response 1s · obtame · d . th st wi usual imulus. One of the following could be the reason:

1· Coldness of feet; test should be repeated after warming the feet.

Cawes of upgoing plantar

2· Sensory loss over the S dermatome

1.

3· Paralysis of the muscle~ of the great toe

UMN lesion

2. Hypoglycemia 3.

Deep coma

4.

Post epileptic tit

5.

Below the age of one year

4

· Sp_inal shock due to transection of the spmal cord

Abdomin a- 1 Re fl

exes (T8 - T12) The patient 5 I1 Id ins . . ?u be warm and relaxed, lying upme pos1t10 11 · l wit 1 a low pillow support11· 1g

-ad. Draw a pin from lateral part of the the I1e ·d1 · en towards mt me I on either side . It bdoin . J Id be below and para lei with the costal shoU. for upper abdominal . . refl exes . and above 11 13 rcr1ns ' I:] i·allel with the m gumal ligaments for 311d pa ' . . . I0we1• ,abdominal reflexes. Avoid any mJury to the patient. N erve supply d of this area is T8 - T12 bove downwar . from a Interpretation ,

Brisk contraction of muscles of the stimulated area and movement of the umbilicus towards that side is normal response.

, Abdominal reflexes are normally absent in the obese people, old age and multiparous women.

Chapter 6-Nervous System 167 of purpose ful movements. It requires intact motor, sensory and cerebellar system. Loss of coordination is called ataxia which may be cerebellar or sensory - due to loss of sense of position. In the presence of gross motor weakness coordination cannot be tested.

Upper Limb Finger Nose Test Ask the patient to touch with his index finger the tip of his nose and your index finger, alternately, rapidly and repeatedly. Keep your index fi~ger at such a distance that patient has to extend his arm fully to touch it (Fig. 6.79).

, Abdominal reflexes are also absent if there is UMN lesion above their segmental level or if there is LMN lesion of the concerned spinal roots or nerves.

Fig. 6.79: Finger nose test

Perform the test with patient's eyes open and tes1 each arm in turn. . In order to further increase the sensitivity of this test move your finger from place to place. ' . sk the patient to close To test for sensory ataxta a h h the his eyes outstretc h h.is arm and t en touc Fig. 6.78: Eliciting abdominal reflexes

tip of his nose.

Cremasteric Reflex (Lt , 2) h SCratch the inner aspect oft h e upp er part oft Th.e h 1 . · f testes t gh. Normally there is elevatt_on ° · 15 rcnex may be lost in UMN leSwn.

Finger to Finger Test

Anal Reflex (S3 4)

S ' · with a sharp cratch the skin near the anal margm · cter. ob·~ect. There is con tract10n • o f t )1 e anal sp1110

Coordination

It

.,,cans smooth and accurate p erformance h,

. . t to exten d an d abduct his arms Ask the pauen . . f the index fingers h brmg ups o . I d fully an t en "d . l · at first with t 1e h ou h a w1 e circ e together, t r g . I the eyes closed. and then wit 1 eyes open ' . . . to ask the patient [I oordmauon 1s Another test or~ 1 . at first with the eyes kc circles m t 1e air to ma . en with the eyes closed. open and th form these movements .. rson can per t l Norma pe . . • lost movcmcn s If coordmauon is ' smoot I1 Iy.

168 become clumsy an d J·erky, and patient may overshoot the target.

Closure of che eyes has no effect on vision. . cerebe II ar acaxia · ----------------,

Lower Limb Heel Knee Test Patient should lie in the bed. Ask him to place thde · d ownwar heel on his opposite knee and sI1.cl e It . alono the shin to the ankle. Then lift it, making a sem~ircle, place it again on the knee and repeat the movement (Fig. 6.80).

Fig. 6.80: Heel knee test

Another test is to ask the patient to lift the extended leg and touch your index finger with the great toe. · As said earlier, movements are clumsy and jerky if coordination is lost.

Heel-Toe Test of Gait (Tandem Walking) Ask the patient to walk along a straight line so that the heel of one foot comes directly in contact with the toes of the other foot. The rare foot is then advanced so that its heel is then placed in front of the previously front foot (Fig. 6.81). Patient with cerebellar dysfunction is unable to do so and tends to fall towards diseased side.

Differential Diagnosis of Sensory and Cerebellar Ataxia Sensory ataxia is due to the loss of sense of position. Unsteadiness and tests of coordination (finger nose and finger to finger tests) become worse when patient closes the eyes; otherwise loss of sense of position is compensated through

Fig. 6.81 : Tandem walking

Sensory ataxia becomes worse when patient closes the eyes while cerebellar ataxia is not affected. Romberg's sign: Ask the patient to stand wit_h his feet close together. A patient of sens01y ataxia · steady when eyes are opened and becornes is t UnS eady when eyes are closed. (A patient of cerebellar ataxia is equally unsteady whether eyes are opened or closed).

-==~: : : : : : - - -- -- - - --== -- - ~C:_!h~a~p~te~r~6::!N~e::r~vo~u~s~S2'.y~st~em~_1~6~9~- --' l 1 JJtVO untary Movemen ts I----------------~

f rernors fhese are rhythmic in:oluntary movement s from alternatmg contraction and result jnu o reI;1,'\c·ation of groups of muscles. These involve eripheral parts of the body like hands, head and p aLJe Jn order to look for tremors in the hand COi1ti · , the patient to outstretch the arms and abduct k as the fingers. If tremors are still not obvious but suspected, place a piece of paper on the dorsum of the hands and observe its movements . Remember: movement s of the paper could be due to wind or a running fan rather than tremors.

l

~

Fig. 6.82: Flapping tremor

Causes

Titubation s

Anxiety: Tremors are fine and become obvious only when arms are outstretche d and fingers are spread. Hands are sweaty but cold.

These are tremors of the head, either to and fro or rotatory, seen in cerebellar dysfunction; may occur as a part of essential tremors.

Thyrotoxicosis: Tremors are similar to those of anxiety but hands are sweaty and warm.

Ties or Habit Spasms

Essential familial tremors: Tremors are coarse and are present, both, at rest and during activity.

These are repetitive and stereotyped movements - the same movement is repeated again and again. Facial grimaces are a common example.

Senile tremors: These are similar to essential familial tremors; occur in old age. Parkinsonian tremors: These are slow and coarse. Typically, there are pill rolling movements of the thumb. Tremors are partially suppressed during voluntary movement s and disappear during sleep. Other features of Parkinsoni sm (rigidity, hypokinesia) are present. Intention tremors: Ask the patient to catch an object, say, a pencil held in your hand. Tremors are absent at rest, become prominent as patient approaches the object and disappear thereafter. Intention tremors are a feature of cerebellar dysfunction . Flapping tremors: Ask the patient to out st retch arms and dorsiflex hands at wrists. Jerky lllovernems of the hands occur due to flexion and extension of the wrists and fingers. Cause_s of fla PPing · tremors are respiratory, rena,/ henattc r . and ea r;d'tac fiailures. To detect · mors 111 flappmg tre an un . . . nt hold h conscious or uncoopcra ttve patte ' . the Patient's arm with one hand and dorsiflcx his and d . .. · h the other (F· an mamtain that pos1t1on wit tg. 6,82).

Choreifor m Movement s These are semipurposive movements which look like fragments of normal movements, but are repeated in a disorderly manner. Movement!tend to move from one part of the musculature to another in quick succession which differentiates them from ties. These occur in Huntington's chorea and rheumatic fever (Sydenham's chorea).

Athetoid Movemen ts These are slow writhing movements princ~pally affecting the distal parts of the hmb_s. . · of choreiform and athetm d Com b mauon . movements may occur in the same pauent. Myoclonic Jerks . en shock like contracuon s that Tl1ese are Sudd · b . lve one or more muscles or a whok hm . mvo · · I TI es' These. can occur singly or rcpcuuvc y. . i _ c.: sometimes occur in normal pcopk wl~c~ talh~g asleep; are also a feature of epilepsy, d!ff11se bram

da/llage or dementia.

170 weakness, as in rnyoparhies. This also occurs in the congenital dislocation ef hip joints.

H emiballismus There is sudden, violent, flail like throwing movement of the limbs on one side. Lesion is in the contralateral subthalamic nucleus.

Parkinsonian Gait Patient bends forward with flexion at the hips and knees. Arms are flexed at the elbows and adducted at the shoulder; there are no associated movements during walking. Initially walk is slow with short rapid steps, feet dragging or sliding along the floor (shuffling gait). As the upper body gradually leans further ahead of the feet, the speed is increased in an attempt to maintain an upright posture (festinant gait).

D ystonic Movements (Torsion Spasms) These are similar to the athetoid movements but involve proximal parts; there are turning or twisting movements oflimbs or trunk. Sustained abnormal contractures and limb posturing may result. Spasmodic torticollis and dystonia musculorum deformans are the examples.

Spasmodic Torticollis It is a type of torsion spasms. These are repetitive rotatory movements of the head and neck to one side, may be accompanied by e:x.'tension of the neck.

Apraxia It means inability to perform learned act in the absence of incoordination, weakness or sensory deficit. Ask the patient to carry out commonly performed acts like combing the hair, buttoning the shirt, or drawing square or triangle on the paper. Patient with apraxia will not be able to carry out these acts. Lesion is in the dominant parietal lobe if apraxia is bilateral and in the non-dominant parietal lobe if apraxia is of the non-dominant limb only.

Gait Ask the patient to walk in a straight line and observe the gait. Following are some of the abnormal types of gait.

Spastic Gait This is seen in UMN paraplegia. Patient does not lift his feet from the ground completely so that toes remain in contact with the ground. Legs swing outward and forward in a circular fashion. Hemiplegic gait is a spastic gait in which only one leg is affected.

Differential diagnosis of upper motor neuron paralysis and lower motor neuron paralysis

High Stepping Gait

Feature

LMN paralysis

This is seen in patients with bilateral foot drop as a result of weakness of the extensors of the feet, as in polyneuropathy. Patient lifts the foot high to clear the toes from the ground and then returns it with a loud slapping noise.

UMN paralysis*

Bulk and nutrition

There is no wasting

There is marked wasting

Power

Groups of muscles are involved

Individual muscles are involved

.

Drunken Gait Patient walks on a broad base in a reeling manner. This occurs in cerebellar lesion. In unilateral lesion patient tends to stagger towards the affected side.

Waddling Gait !he body sw~ys from si~e to si~e as each step 1s taken. This occurs Ill proximal muscular

'

Tone

-

It is increased It is decreased

-

*

Neuronal shock: When there is sudden damage to the UMN system, as 111 · b rain hernorrhage, anreno · r Iiorn cells are d b "_ epressed. Weakness is accompante,d Y hypoton1a' 'a11d ,l- b.sent tendon reflexes; p Iantat· 1·s usually upgoiiig. TI11s · 1s . called neuronal (or sp1na · I) s I1ock T, · I ' fi I . yp1ca features of UMN lesion appear after a ew 1ours to days.

~=~;=~~ ~~~=~~====~- : - - - - - -~C~h~ap~t::_e~r6~~N~e~rv~o~u~s1Stys~te~m~J1]_7~1_ _ These are

, fendon jerks

v----

brisk

These are diminished or absent

It is upgoing It is downgoing (Babinski's (Babinski's sign sign 1s is negative) positive)

plantar

These may be These are absent present (these and are absent if cremastenc reflexes concerned spinal roots or nerves are affected) Absent Fasci cu Iati ons 1May be present

Abdominal

-

LOCALIZATION OF MOTOR LESION Upper Motor Neuron Lesion The cardinal signs of UMN damage are hypertonia, hyperreflexia and upgoing plantar. Manifestations of lesions at various sites along the course of UMN pathway are given below. The site of lesion may be:

hemiplegia is on tl1 1 ·d f . e ot 1 er si e o cra111al ne I er . I . rve pa sy. ama nerve mvol I 1. vement oca 1zed. For example:

.

side. Lesion is on the . Dependmg upon the . 1es1on can be further

• •

If3rdnerve is involved, lesion is in the midbrain. If 6th or 7th · ·

•

If9 th or 10 th

nerve is mvolved, lesion is in the pons. ·

·

nerves 1s mvolved lesion is in the medulla oblongata.

Spinal Cord Upper motor neuron damage is usually bilateral. If it is unilateral, lesion is on the side of motor weakness.

•

If upper limbs are also involved, lesion is above the CS spinal segment.

• If all

the abdominal reflexes are absent, lesion is above the T8 spinal segment.

• If

there is evidence of lower motor involvement - like wasting- in the segmental distribution, lesion is at that segment.

•

If there is sensory loss in a dermatome,

1. Motor cortex

lesion is at that spinal segment.

2. Internal capsule 3. Brain stem 4. Spinal cord

•

If sensory tracts are involved, there is sensory loss up to a certain level; the actual site of lesion is a few segments above that depicted by the sensory level.

Motor Cortex

Hemisection of the spinal cord (Fig. 6.83, 6.84)

As motor area is spread over a large area, cortical lesion usually gives rise to monoplegia rather ~han hemiplegia. Other manifestations like apraxia_ or agnosia may also be present. There are specific rnanifestations due to lesions of various lobes, ~-g., there is inferior quadrantanopia if lesion I5 . • US in the parietal lobe; there 1s homonymo hemianopia iflesion is in the occipital lobe; grasp refl_ex is present and the patient is emotionally labile if the lesion is in the frontal lobe.

Below the level of the lesion there is: • Jpsilateral UMN weakness and loss of sense of position and vibration • Contralateral loss of sense of pain and temperature This is called Brown-S ndrome

Posterior ---.... column Lateral cortico spinal tract

Inte tna 1 Capsul e

~

C----1

As both the motor and sensory fibers are very c~osely packed in the internal capsule, its lesion gives rise · to dense hem1plcgia . · an d f:a cial nerve . Palsy 0 f th c opposite . side . ( uncrosse d I1 e miplcg1a).

llr ain · Stem

!n brain stem lesions I.e.

.

there is crossed hcmiplcgiad, . c side an ' cranial nerve palsy 1s on on

.

Lateral spinothalamic tract

'

.

. svl·rse section of th e spinal cord ;

.

Fig. 6.83. Tr:"'- . . ·ts invol\'ed in hcnuscc tton shaded area md1rat111g tr,1l .

~

172

•

D eviatio n of che angle of the mouth due to associated fac ia_l nerve palsy can be detected by applymg pressure over the supraorbital notch; the angle deviates to the healthy side.

•

Bilateral upgoing plantars in a deeply comatosed patient have no localizing value, but if plantar is upgoing only on one side, it is the most useful sign of hemiplegia.

Lower Motor Neuron Lesion The cardinal signs of LMN damage are wasting of muscles, hypotonia, diminished or absent reflexes and downgoing plantar. Manifestations of lesions at various sites along the course of LMN pathway are given below. The site oflesion may be: 1.

Nuclei of cranial nerves

2.

Anterior horn cells

3. Nerve roots 4. Nerves (cranial or peripheral) If nuclei of cranial nerves are involved, 0 as in local lesions of brain stem, there is paralysis of muscles supplied by the affected nerves. Manifestations are similar if cranial nerves themselves are involved along their course.

Fig. 6.84: Manifestations of hemisection of the spinal cord: Pyramidal signs and loss of position and vibration on the same side (vertical shade); loss of pain and temperature on the opposite side (horizontal shade)

0

If anterior horn cells are involved, as in poliomyelitis or motor neuron disease, manifestations are widespread like monoparesis, parapares1s or quadriparesis.

o

If a root is involved the muscles ' supplied by that root are paralyzed, e.g., If T1 root is damaged, there is paralysis of all the small muscles of the hand.

0

If a single peripheral nerve is involved muscles supplied by that ne~e are affected, e.g., in radial nerve paralysis there is weakness of the extensors of the wrist resulting in wrist drop. If multip_le peripheral nerves are involved as Ill neuropathy, muscles of distal parts of the limbs are affected. In post infective polyneuritis (Cui/lain Barre syndrome) there is paraplegia or quadriplegia.

Hemiplegia in a comatosed patient Detection of hemiplegia due to a recent stroke in a comatosed patient may be difficult. Following signs are helpful.

•

Look for hypotonia; this may be the only evidence of hemiplegia.

•

Raise the arm of the patient and let it fall. If it is paralyzed it falls as if it did not belong to the patient; it may even hit the face of the patient. The sound arm does not fall in that way.

-------------~- - - - - - -- - - -- - - - _-2C:!:h~a£pt~e~r ~6=-!N~e~r~vo~u~s~S~y~st~e~m~ ~l7[:_3~ - · k c Diseases of Muscles

In diseases of muscles (myopathies) weakness is more marked in the proximal muscles, e.g., rnuscles of shoulder and pe lvic girdles. Affected 111 uscles are usually wasted but fasciculations are absent and reflexes are preserved. In Duchenne muscular dystrophy there is pseudohypertrophy.

~ n muscle diseases reflexes are normal.

In 111 yotonic dystrophy relaxation of the muscles is defective. Ask the patient to grip your hand and rhen let it go suddenly. He will only release the hand slowly. Strike the muscle lightly over thenar eminence or tongue with the tendon hammer. A dimple of contraction will appear which will disappear only slowly.

In 111yasthenia gravis (a disease of neuromuscular junction) extraocular and bulbar muscles are commonly involved. The weakness becomes more marked after repeated contractions of muscles. Ask the patient to count till hundred;

t11ne ta en ior the last 50 will be more than the time taken for the first 50. Another test is to ask the pa_tient to look up; ptosis will develop after sometime.

Hysterical paralysis

Hoover's sign: The patient should lie supine with legs extended. Place a hand under one heel and ask him to lift the opposite leg against resistance. If the leg with your hand under its heel is normal, it will be pressed downwards, but if paralyzed, it will not be pressed. If paralysis is hysterical the leg will be pressed down more strongly than when patient is asked to press down voluntarily. Babinski's rising up sign: Patient should lie on the back. Ask him to sit up without support of his arms. In organic spastic paralysis, paralyzed leg is flexed at hip and is lifted from the bed while heel of the normal leg is pressed down. This phenomenon does not occur in hysterical paralysis.

Differential Diagnosis of Motor Neuron Disease, Neuropathy and Myopathy Features

Motor Neuron Disease

Neuropathy

Myopathy

Wasting

It is marked

It is marked

It is marked. In some varieties there is pseudo hypertrophy

All groups of muscles are involved

Distal muscles are involved

Mainly proximal muscles are involved

Fasciculations

These are characteristic of motor neuron disease

These are absent except in acute neuropathy

These are absent

Sensory loss

It is never present

It is almost always present

It is never present

Retlexcs

Diminished in progressive muscular atrophy and brisk in amyotrophic lateral sclerosis

Diminished or absent

These are normal

I

Muscles I involved

I,.....__ Pl an tars I

Downgoing in progress ive mu scu lar atrophy a nd upgoing in amyotrophic lateral sc lerosis

Down going

Downgoi11g

-

-

174 •

SENSORY SYSTEM Sensations are of two types; primary and cortical. Primary sensations are touch , pain, temperature, position, passive movements and vibrations. Cortical sensations are localization, two point discrimination, stereognosis and graphesthesia.

•

normal sensation. •

Explain to the patient what you are going to do and how he should respond.

Compare two sides and ask the patient whether sensations are equal on both sides or not.

•

Primary Sensations • Expose the area to be examined .

Appl y stimulus to a possible normal site like sternum so that he can experience the

Don't duplicate the tests as repetition results in loss of patient's cooperation, and information obtained may be conflicting and variable .

• • •

•

•

•

•

• • Fig. 6.85: Sites to be tested anteriorly

•

. to b Fig. 6.86: Sites e tested posteriorly

~ - - - - - -- - - - - - - - - - - - - - - - - -~C~h~ap~t~e~ r ~6:=!N~e::r~vo~u~s~S~y~s~ te:::m~_!.17_715_ __ • To map the area of abnormal sensations, at Pain first examine abnormal area and then move towards normal area. Use a di sposable pin (or hypodermi c needl e if pin is not avail able) to avoid transmiss ion • The sites tested should cover the territories of infectio ns like hepatitis B and C. At first, 0 [, both, peripheral nerves as well as touch the patient with both ends of the pin at a posterior nerve roots. These are shown in presumably normal site to make him experience fig. 6.85 and 6.86. what you mean by 'sharp' and 'blunt'. Then ask Sensations may be completely lost (anestliesia), him to close the eyes, touch him with sharp and impaired (/1ypoesth esia) or h eightened (dysestliesia). blunt ends of the pin in a random sequence and ensory symptoms are described on page 117. see whether he can differentiate between the two or not (Fig. 6.88). If patient can feel but cannot Touch distinguish between sharp and blunt, it means his sense of touch is intact but sense of pain is Touch the skin with a small point of cotton lost. wool or a piece of paper (Fig. 6.87). (Don't move the touching object over the skin). In order to standardize quantity of the stimulus a monofilament is used nowadays which when pressed against the skin transmits about 10 gram of weight. Ask the patient to close his eyes, and raise his finger, say yes or count when he feels the touching object. He should also tell whether sensations are similar on both sides or different.

Fig. 6.88: Testing pain in hand and foot

Temperature '] k two test tubes containing cold and hot (not a e hot) water and app Iy to a Iic::i , ltlt ~, p1rt ' l) th.1t vcr '( t cxpe1·1·e11ccs the c.litTereucc . 1 hen ,1ppl , , ,1 · Pat1en , . 1 s"111 to tic thee tubes Jll a I.,cll1 do111 •SC(!llCIJCC , . , ·t tl) br' tested ,1110 ,\ ·k lrnn to md1 catc ot1cpa1 '" · . < rI whether it is hot or ·old (Fig. 6.8)). Fig. 6.87: Testing touc h in hand and foot

176 this purpose. T his is the most commonly employed test (Fig. 6 .90).

Fig. 6.89: Testing temperature

Deep Pain Squeeze patient's muscles and tendons and as~him to indicate when the pressure becomes pamful. You have to decide whether the force applied could be painful in a normal person or not.

Sense of Position and Passive Movements There are a number of ways of testing sense of position and passive movements. 1.

2.

Ask the patient to close the eyes. After random movements in different direction, place patient's limb in a particular position, m aking sure that it does not touch the body, and ask him to imitate it with the other limb. If sense of position is intact, he will bring the other limb in exactly the same position. At first, show the patient up and down movem ents of the great toe. Then stabilize the proximal phalanx of the great toe by grasping it between thumb and index finge r of your left hand. Grasp the terminal phalanx of the great toe on its lateral sides between thumb and index finger of your right hand. It should not be in contact with the other toes. Ask th e patient to close the eyes. M ove the terminal phalanx, gently and slowly, up and down in a random sequence so that patient ca nn ot guess, and ask him to id enti fy th e directi on of movem ent. Repeat the test o n co ntralateral sid e. In upper limb, termin al ph alanx of index fin ger is used for

Fig. 6.90: Testing sense of position and passive move ments in hand and foo t

3.

Move a part of the body (toe or limb) and ask the patient to indicate as soon as he recognizes the movement. Note the angle through which part has moved. Normally movement ofless than 10° can be recognized.

Other Features of Impaired Sense of Position

1.

Patient may complain of unsteadiness during darkness.

2.

Ask the patient to outstretch the arms and close the eyes· there are involuntary ' . I movements of the affected arm whic 1 disappear on opening the eyes .

3.

Tests of coordination (page 167) deterior_ate on closing the eyes and Romberg's 5,gn (page 168) is positive.

Sense ofVibration Take a tuning fork with frequency of 128 cycles

Chapter 6-Nervous S stem 177 . •conds. For setting it into vibration, e ither . P •'ke it on a rubber pad or side of your kn ee . At 5tt 1 _ place the base of vibrating and still tuning fi1 st, . 1·k c l1ead ·konaproxima lb onyprommence 1 e iore fot "t patient can e;,..rpenence . .b . Th v1 rations. en so tIl:s l ltt I raise d 1ntracra111:1 . . ,!ttl' tlJ 11 n: 111 .1(11 rc of sut11r,-ysm al nocturnal 9 D ystonic m ovem ents 170

E Ecchymosi~ 25 Echolalia 127 Edem a 8, 22 causes of 22 non-pitting 22 pitting 22 E isenmenger's syndrome 63 Ejectio n systo lic clicks 53 aortic 53 causes of 53 pulm o nary 53 Emphysem a subcutaneou s 24

Dyslexia 129

Enteric fever sample h istory of 2 11

D ysphagia 10, 92 glo bus hyste ricus 93 in esophageal stricture 92 in neuromuscular disorders

E 1-ythe m a m arginacum 25 n odosum 25

93 D ysphasia anomic 126, 131 Broca's 130 conductio n 126, 130 expressive 125 flue nt 126 glo bal 126, 130 isolation 126, 131 m otor 125, 130 no n-flue nt 125 receptive 126 sen sory 126, 129 transcortical m otor 126, 130 transcortical sensory 126, 129 Wernicke's 129 D yspho nia 127 D yspnea 8

Examination develo pmental 207 general physical summar y of 25 writing out 28 n eonatal 205 of abducent nerve 139 of alimentary syste m writing out 114 of alimentary syste m summary of 113 of autonomic nervous system

182 of cardiovascular system in child ren 197 writing out 72 of cardiovascular system summary of 71 of facial nerve

m otor function 145 of nervous system 123 summary of 183 of precordium 43 in children 198 o f respirato1-y system writing out 90 of re piratory system summary of 89 ofspeech 127 of taste 146 of troc hlear nerve 139 pediatric 187, 191 fa,.l)ressive dysphasia 125 Extremities in children 197 in newbo rn 206 Eyes in n ewborn 206

F Face in newborn 205 Facial n erve examinatio n of motor function 145 interpretatio n of 146 paralysis o f LMN type 146 UMN type 146 Facial palsy in children 203 in newborn 206 Fahrenheit scale 6 Fallot's tetralogy 63 Fasciculatio n s 154 Fecal masses in children 201 Feeding 188 Feet 22 in children 197 Fever 6 associated sym ptom s 8 continuo u s 8

Index 217 grad e 6 in childre n 188 inte rmitte nt 8 m ode o f o n set 6 patte rn 8 quartan 8 quotidian 8 relapsing 8 remittent 8 rigo rs o r chills 6 tertian 8

in children 201 in newbo rn 206 G estational age 2 06 G lobal d ysphasia 126, 130 G lo bus hyste ricu s 93 Graham Stee l murmu r 63 Groin examinatio n of 11 2

uncr definition of 155 Hemo

l'.

ea

· o•- 7duiercnaal diagn --- of 9"' l'

H

0

Hem, I _·a 11 cro-sed definition of 155 definition of 1.33

G ower' sign 205

Fits 11 in c hildre n 189

-

or

HemL1 e igasaic 99

169

Flue nt d ysph as ia 126

H abit spasm

Fluid thrill 110

H air di rriburion ">

Fontan e! ante rio r bulging 204 Fo rced expirato ry ti m e

Hem1baJlismu

pubic 99 Hand in children 191

Forced eAl)iratory \·olume in o n e second 90

Harri on·

Forced vital capacity 90

Headache 11

Frictio n sound , in abdomen 112

ulcu

clu ter 11 psych ogenic 11 Head growth 202

G Gait 170 drunken 170 festi nant 170 h emiplcgic 170 high stepping 170 in child ren 189, 203 parki nsoni an 170 shu ffli ng 170 spas tic 170 waddling 170 G all bladder e nlargem e nt, causes of 104 mucocele 104

Hernial oririce 99 Higher mental function 12-l-

HaJico i 2 7

raraumbilical 99 umbilical 99

Head in newborn 20.3 H earing in c hi ld ren 190. 203 H eart rate in chi ldre n 197 in newb orn 206 H eart sound second splitting of fixed 5 1 reverse 51 third in children 198 H eig h t 192

G ang lio n ge ni culate 147

H em atem esis 93

Geniculate ganglio n 147

H em aturia 10

G e nitalia examinatio n of 112

H emiano p ia binasal 136

H em ato m a 25

Hip di locatable 206 H ir eh pring· disease 202 Hi cory d evelopme ntal 191 e nvi ronme ntal 191 example no. 1 209 fam ily .3, 191 in children 187 information fro m ano ther pe rso n 4 menst rual 4 no. 2 2 10 110. 3 211 occupatio nal 5 of birth 190 antenatal 190 natal 190 newborn 190 postnatal 190 offeeding 190 of immunizatio n 190 of presen t illness in children 187 past 4, 191 pe rson al 5, 19 1 record 12 social 5, 19 1 treatme nt 4

218 H oarseness in children 202 H oover 's sign 173 Hum, venous in the abdomen 112

Ischemia acute 72 ch ronic, signs of 72 I olation dy phasia 126, 131

Hydration 23 H yperpyrexia 6 H ypertensio n in children 198

J aundice 10, 24 in child ren 189 physiological 205

H ypertonia 155 in children 203

J oint pain in 11

di fference between traumatic lumbar puncture and subarachno id hem orrhage 186 indications of 185 diagnostic 186 therapeutic 186 Lumbrical 156 Lung fu nction tests 90 in obstructive lung diseases 90 in res trictive lung diseases 90

H ypertrophi c obstructive cardi- Jugular veno us pulse om yopathy 63 cannon waves 42 rapid 'y' descent 43 H ypertrophy 154 ventricularization of venous H ypospadias is 201 pulse 43 Hypotherm ia 6

Lymph nodes drai nage area 22 of groin 22

H ypo to ni a 155 in children 203

M acules 24

H ysterical paralysis 173

I Indications oflumbar puncture 185 diagnostic 186 therapeutic 186 Infancy 187

K Kernig's sign in children 204 kidneys palpable, cau ses of 107 Koplik's spots 196 Kussmaul sign 43

Inspection of precordium 43 in children 198 Intercostal spaces indrawing of in newborn 206 Internal capsule lesio n of 171

M ass 8 in rectum 11 2 M easuremen t of the circumfere nce of limb 154 M easurem ents in children 192 M eningeal irritati on signs of in children 204

Kyphoscoli osis thoracic 78

Infant acutely ill 208

M

L

M eningism 204 M ethem oglobin 23

Left ventricular fa ilure sample hi sto ry of 209 Length 192 Lethargy in chi ldren 189 Light reflex 138 Liver in children 201 in new born 206

Interpretation of 3rd, 4th, 6th nerves lesions 139 of facia l nerve lesion 146

Localizatio n of lesion in motor system 171

lntussuscep tion 201 Involuntar y movem ents in children 189

Lumbar puncture 185 com pl ications of 186 contraindications of 186

Migraine 11 Milesto nes 207 eighteen months 208 nine mo nths 207 six m onths 207 six weeks 207 three m onths 207 twelve mon ths 208 M onoplegia 11 defini tion of 155 Motor cortex lesion of 171 Motor dysphasia 125, 130 M otor system

Index 219 in children 203 Movements in children 203 Murmur Austin Flint 63 Carry- Coomb's 63 cau ses of 55 early diastolic causes of 55 grades of 56 Graham Steel 63 in newborn 206 inten sity of 56 pansystolic causes of 154 Murphy's sign 104 Musculo-skele tal system 204 Myasthenia gravis 173 M yoclonic j erks 169 Myopathies 173 M yotonic dy t rophy 1 3

Newborn at d elivery 205 at six weeks 206 d uri ng first week ofl ife 205 Nod ules 25 Non-flue nt dysphasia 125 Nose in children 195 Nystagrnus 141

0

N eck in childre n 196 re traction 196 webbing 196 N eck rigidity in child re n 204 Neck veins in children 198 N eonatal examinatio n 205 N eon atal pe riod 187 N erves cranial. see c ranial nerves in children 202 N e rvous system autonomic examination of 182 examination of 123 in child ren 202 in newborn 206 N euronal shock 170

of trachea - 9

Palpicicion 9 Papules Parah 11 o -sewmh cranial nerw ~ ~type:~ c~~rype

Paralytic ileus 111 Para legia 11 derinicion o f 155

Odors abnormal 2-l-

Par

Optic chiasma ,; u al field dere . due co lesion or- 13

O ral ca,;t\• in children 196 Orthopnea 9 0-·arian cyst percu sion for 111

N

or- precordium 43 in children 198 or- leen 105

p

11

Peak e:-,..-pirato ry flow rate 90 Pecru excaYarum 77 Ped iarric exami natio n 187 Pepric u lcer ample hi rory of 210 Percu ion for OYarian cyst 111 of abdomen in children 201 of precord ium in children 198 tidal 4

Pain 5 aggravating facto rs 6 associated phen om e no n 6 character 5 duration 5 frequency 6 intensity 5 in the joint 11 pe riodicity 6 radiation 5 referred 5 relieving fac tors 6 shift of 5 site 5 special times of occurrence 6

Pe rineum in children 201

Palilalia 127

Perisylvian area 126

Pallor 23

Petechiae 25

Palpation of abdomen in children 200 of chest 79

Pigmentation 24

Percu ssion n ote d u ll -lhyperresonant 84 impaired 84 resonant 84 stony dull 84 tympanitic 84 types of 84 Perianal dermatitis 201 Pericardia! knock 53

P leural effu sion aspiration of 90 cau ses of 90

220

R

Pleural rub 87 Polyuri a 10 Posture in childre n 189 Power of muscles 155 grades of 156 in childre n 203 Precord ium auscultation of in childre n 198 bulging of 43 examin atio n of 43 in childre n 198 inspection of 43 in childre n 198 palpati on of 43 in childre n 198 percuss ion of in childre n 198 promin ent veins 43 pulsatio n 43 scars 43 Prescho ol child 187 Present ing compla ints in childre n 187 Prostat e 112 Pseudo hypertr ophy 154 Pulmo nary ej ection systo li c click 53 regurgi tation 61 Pulse characteri stics of 36 in childre n 197 poste rior tibia! 31 rate 32 Purpur a 25 Pustules 25 Pyloric stenosi s 201 Pyloric tumor 201

Q Quadri plegia d efinitio n of 155

Rombe rg's sign 168

Ramsay Hun"t synd rome 147

Ronchi 86 causes of 86

Ras h in childre n 189

Root irritatio n signs of 181

R aynaud 's p heno m eno n 72

Rub pleural 87

Recept ive dyspha sia 126 Rectal exam inatio n 112

s

Rectal prolap e 201 Refl ex accomm odation 139 gras p 204 palmar 204 plantar 204 lig h t 138 Moro 204 plantar in childre n 203 rooting 204 sucking 204 swallow ing 204 tonic neck 204 Reflexe s infanti le 204 neonatal 204 Pupilla ry 141 root value of 162 supe rficial in children 203 Respira tio n in newbo rn 206 Re piratory failure 91 type I 91 causes of 91 type II 91 causes of 91 Respira tory rate 23 in newbo rn 206 Respi ratory system exam inati on of sum mar y of 89 writing out 90 Rigidit y 155 cog-wh ee l type 155 hysterica l 155 lead pipe type 155

calcs 25 School child 187 Seizure in chi ldren 189 Sensor y d ysphas ia 126, 129 Senso1y system in ch ildre n 204 Sign Babins ki's rising up 173 Brudz inski 's 204 Chvost ek's 182 Gower 's 205 H oover's 173 Kernig 's 204 Kussma ul 43 Trouss eau 's 182 Sign of chronic ischem ia 72 deep venous thromb osis 72 root irritatio n 181 Skin in newbo rn 205 lesio ns, de fi nitio ns of 24 Sound abno rm al 24 Spastic ity 155 clasp knife type 155 Speech articula tion 127 de layed 202 disorde rs, miscell aneous 127 distu rbances 129 examin atio n of 127 in ch ildren 202 nasal in childre n 202

scanning 126 slurring 126 Spider nevi 25 Spina bifida 197 Spinal cord hemiseccion of 171 le ion of 17 1 Spine in children 197 Spirometry 90 Spleen in children 201 palpation of 105 Splitting of S2 fixed 51 in children 198 reverse 51 Sputum 73 Squint in children 202

general 3 locomotor system .! nervous system 4 respiratory system 3 skin 4 urinary system 3

T Tachycardia 32 causes of 33 Taste exam ination of 146 Teeth in children 196

1

lI Umbihcu in ne,,·bo n~ _ Uncon c10u nc.: . in children l '9

Tendon jerks in chi ldren 203

Stridor 86

Thorax in children 197

Systemic inquiry alimentary system 3 cardiovascular system 3 endocrine 4

·

Urinary bladder in newborn 206

Tetraplegia definition of 155

Symptoms in children 187 of cardiovascular system 29 of deep venous thrombosis 72 routine questions about 5

E9

··

Temperature 23 diurnal variation 23

Strabismus in chi ldren 202

Summary of examination general physical 25 of alimentary system 113 of cardiovascular system 7 1 of nervous system 183 of respiratory system 89

Trnu~u·

:i

Upper motor neuron I 171

Testes undescended 201

Sulfhemoglobin 23

examuua

Telangiectases 25

Stammering 127

Succussion splash in abdomen 111 in chest 87

169

V Venou hum in the abdomen 112 Venous Hum 57 Venous system 72 Ventricularizacion of venous pulse 43

Thrill causes of 47

Vesicle

Thrombosis deep venous 72

Vesicular breaching with prolonged expiration

Thrush 196

Vessel ,vall condition of 35

Ties 169 Titubations 169 Tone of muscles 155 in children 203 Tonsil 196 Torsion spasms 170 Torticollis, spasm odic 170 Tracheal tug 79 Transcortical motor dysphasia

126, 130 'TI-anscortical sensory dysphasia 126, 129

25

Vision in chi ldren 202 Visual field defects due to optic chiasma 136 Visual inattention 135 Vitiligo 24 Vocal resonance 87 Voice in children 202 Vomiting 9, 93 in children 188

f.

222

w Walking independent in children 203 Wasting 154 Weakne s 11 Weight 192 loss of 8 Wernicke s dysphasia 129 Wheals 25 Whispering pectoriloquy 87 causes of 87 Word blindn ess 126, 131 Word deafness 126, 131

X Xanthochromia 186

Bedside Techniques Methods of Clinical Examination

Bedside Techniques: Methods of Clinical Examination is a distinguished book, explaining the causes, symptoms and physical · signs specifically preferring local prevalence of diseases. The sequence of description in this book is in accordance with the local teaching practices and the methods have been described in simple language. A large number of illustrations have been included to help reader understand various examination techniques. This book provides essential information required by undergraduate and postgraduate students.

Dr. Mohammad Inayatullah previously served as a Professor of Medicine at Nishtar Medical College, Multan. Currently, he is serving as a Professor at Multan Medical and Dental College, Multan. He is also a Fellow and Master of Royal College of Physicians, London. He has authored two other books; Essentials of Differential Diagnosis and Treatment Guide.

Bedside Techniques

Methods of Clinical Examination

Muhammad Inayatullah Shabbir Ahmed Nasir

Paramount Books

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