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K27185_C000.indd 2 22/06/2018 15:19
 Complete OSCE Skills for
Medical and Surgical Finals
Second Edition

Edited by

KATE TATHAM BSc (Hons) MBBS PhD MRCP FRCA FFICM

Specialty Registrar in Anaesthetics and Intensive Care,
Imperial School of Anaesthesia;
Clinical Lecturer, Section of Anaesthetics,
Pain Medicine and Intensive Care, Imperial College,
London, UK

KINESH PATEL BA (Hons) MBBS MD MRCP

Consultant Gastroenterologist,
Chelsea and Westminster Hospital NHS Foundation Trust,
London, UK

K27185_C000.indd 3 22/06/2018 15:19

 CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742

© 2019 Kate Tatham and Kinesh Patel

No claim to original U.S. Government works

Printed on acid-free paper

International Standard Book Number-13: 978-1-498-75020-2 (Paperback)

International Standard Book Number-13: 978-1-138-09982-1 (Hardback)

This book contains information obtained from authentic and highly regarded sources. Reasonable
efforts have been made to publish reliable data and information, but the author and publisher cannot
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publishers have attempted to trace the copyright holders of all material reproduced in this publication
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Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced,
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Visit the Taylor & Francis Web site at

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and the CRC Press Web site at

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K27185_C000.indd 4 22/06/2018 15:19

 Contents

Preface ix
List of contributors xi
List of abbreviations xiii

1 History1
Catherine Bennett
2 Examination: Cardiovascular 27
Kate Tatham and Kinesh Patel
3 Examination: Respiratory 43
Kate Tatham and Kinesh Patel
4 Examination: Abdominal 59
Kate Tatham and Kinesh Patel
5 Examination: Neurological 79
Kate Tatham and Kinesh Patel
6 Examination: Musculoskeletal 113
Kate Tatham and Kinesh Patel
7 Examination: Surgical 143
Paolo Sorelli
8 Examination: Endocrine 153
Kate Tatham and Kinesh Patel
9 Examination: Dermatological 165
Kate Tatham and Kinesh Patel
10 Obstetrics and Gynaecology 175
Rebecca Evans-Jones
11 Genitourinary Medicine 205
Catherine Bennett
12 Paediatrics213
Sarita Depani

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 vi    C o n t e n t s

13 Procedures225
Heidi Artis and James R. Waller
14 Emergencies257
Heidi Artis and James R. Waller
15 Interpretation of Data 269
Lucy Hicks
16 Communication skills 301
Heidi Artis and James R. Waller

Appendix 319
NEWS observation chart
Index 321

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 To our families

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K27185_C000.indd 8 22/06/2018 15:19
 Preface

Clinical examinations are a stressful but necessary part of medical school finals. However,
with the appropriate preparation and practice, they can become significantly less daunting
and even an opportunity to prove your clinical skills.
The aim of this book is to help in this process of revision by providing an overview of
common clinical situations encountered in OSCE stations. This quick reference text allows
you and your peers to test each other’s skills both at the bedside and in role play scenarios.
Although this book has not been written as an exhaustive guide, it provides the essential
knowledge necessary to succeed in your exams.
Good luck!
Kate Tatham and Kinesh Patel

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K27185_C000.indd 10 22/06/2018 15:19
 List of Contributors

Dr Heidi Artis BA (Hons) MBBS FRCA

Specialty Registrar in Anaesthetics, University Hospital Southampton, UK
Dr Catherine Bennett BSc (Hons) MBBS MRCGP DFSRH DRCOG
General Practitioner, Wiltshire; Clinical Evidence Fellow, West of England Academic
Health Science Network, UK
Dr Sarita Depani BSc (Hons) MBBS MSc MRCPCH
Cancer Research UK Paediatric Oncology Clinical Trials Fellow, Great Ormond Street
Hospital for Children NHS Foundation Trust, London & Birmingham University Clinical
Trials Unit, UK
Miss Rebecca Evans-Jones BA (Hons) MBBS MSc MRCOG DTM&H
Consultant in Obstetrics and Gynaecology, Gloucestershire Hospitals NHS Foundation
Trust, UK
Dr Lucy Hicks BSc (Hons) MBBS MRCP FHEA
Specialty Registrar in Gastroenterology and General Medicine, Northwest London, UK
Dr Kinesh Patel BA (Hons) MBBS MD MRCP
Consultant Gastroenterologist, Chelsea and Westminster Hospital NHS Foundation Trust,
London, UK
Mr Paolo Sorelli MBBS MSc FRCS
Consultant Colorectal Surgeon, Lewisham and Greenwich NHS Trust, London, UK
Dr Kate Tatham BSc (Hons) MBBS PhD MRCP FRCA FFICM
Specialty Registrar in Anaesthetics and Intensive Care, Imperial School of Anaesthesia;
Clinical Lecturer, Section of Anaesthetics, Pain Medicine and Intensive Care, Imperial
College, London, UK
Dr James R Waller BSc (Hons) MBBS MRCP
Consultant Cardiologist and Physician, Lymington New Forest Hospital, Southern Health
NHS Foundation Trust, Hampshire, UK

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K27185_C000.indd 12 22/06/2018 15:19
 List of abbreviations

β-hCG β human chorionic gonadotropin

AAA abdominal aortic aneurysm
ABG arterial blood gas
AC air conduction
ACTH adrenocorticotropic hormone
AED automatic external defibrillator
AF atrial fibrillation
AFP α-fetoprotein
ASIS anterior superior iliac spine
BC bone conduction
BCC basal cell carcinoma
BMI body mass index
bpm beats per minute
CABG coronary artery bypass graft
CIN cervical intraepithelial neoplasia
CNS central nervous system
COPD chronic obstructive pulmonary disease
COX-2 cyclo-oxygenase-2
CPR cardiopulmonary resuscitation
CSF cerebrospinal fluid
CT computed tomography
CTG cardiotocograph
DIP distal interphalangeal
DMARD disease-modifying antirheumatic drug
DNACPR do not attempt cardiopulmonary resuscitation
ECG electrocardiogram
ESR erythrocyte sedimentation rate
FBC full blood count
FEV1 forced expiratory volume in 1 second
FiO2 fraction of inspired oxygen
FSH follicle-stimulating hormone
FVC forced vital capacity
GCS Glasgow Coma Scale
GTN glyceryl trinitrate

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 xiv    L i s t o f a b b r e v i a t i o n s

HIV human immunodeficiency virus

HPV human papilloma virus
HRT hormone replacement therapy
HSMN hereditary sensory and motor neuropathy
ICE ideas, concerns and expectations
ICP intracranial pressure
IE infective endocarditis
IPF idiopathic pulmonary fibrosis
IUS intrauterine system
JVP jugular venous pressure
LDH lactate dehydrogenase
LH luteinizing hormone
LMN lower motor neurone
LMP last menstrual period
MCP metacarpophalangeal
MDI metered-dose inhaler
MI myocardial infarction
MMR measles, mumps and rubella
MRI magnetic resonance imaging
NEWS National Early Warning Score
NSAID non-steroidal anti-inflammatory drug
OSA obstructive sleep apnoea
PaCO2  partial pressure of carbon dioxide in arterial blood
PALS Patient Advice and Liaison Service
PaO2  partial pressure of oxygen in arterial blood
PCI percutaneous coronary intervention
PCKD polycystic kidney disease
PCOS polycystic ovary syndrome
PEFR peak expiratory flow rate
PFT pulmonary function test
PID pelvic inflammatory disease
PIP proximal interphalangeal
PND paroxysmal nocturnal dyspnoea
POC products of conception
SCC squamous cell carcinoma
SFH symphysis–fundus height
SFJ saphenofemoral junction
SIADH syndrome of inappropriate antidiuretic hormone secretion
SpO2 peripheral capillary oxygen saturation
STI sexually transmitted infection
U&E urea and electrolytes
UMN upper motor neurone
UTI urinary tract infection

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 HAPTER
C H A P T E R 1

History
CATHERINE BENNETT

History taking skills 1 Tiredness13

Chest pain 4 Headache15
Shortness of breath 5 Collapse or fall 17
Fever/pyrexia of unknown origin 7 Alcohol misuse 19
Abdominal pain 9 Psychiatric history and risk assessment 21
Change in bowel habit/rectal bleeding 12

HISTORY TAKING SKILLS

Familiarity with the key components of a history is invaluable when taking a history from
any patient.

INTRODUCTION
⦁ Introduce yourself
⦁ Ensure the patient is sitting comfortably, alongside, and not behind, a desk
⦁ Confirm the reason for the attendance

PATIENT DETAILS
⦁ Confirm the patient’s details:
• Full name
• Age and date of birth

PRESENTING COMPLAINT
⦁ Ask the patient to describe their problem by using open questions (see Box 1.1)
⦁ The presenting complaint should be expressed in their own words, e.g. ‘heaviness in
the chest’

BOX 1.1 EXAMPLES OF OPEN QUESTIONS

⦁⦁ How can I help today?

⦁⦁ What can I do for you today?
⦁⦁ Why have you come to see me today?
⦁⦁ What seems to be the problem?
⦁⦁ What kind of problems have you been having recently?
⦁⦁ Can you tell me a bit more about that?

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 2    H i s t o r y

⦁ Do not interrupt their first few sentences. Pausing after the patient’s first few sentences
before asking questions can sometimes elicit more information
⦁ Try to draw out their ideas, concerns and expectations (‘ICE’), e.g. ‘Was there anything
that you thought might be causing this or anything in particular you were worried
about?’ or ‘What were you hoping for today?’
• Use active listening techniques, e.g. nodding
• Reflect back patients’ own words/feelings to show you have heard them, e.g. ‘I can
see that you are upset by that,’ or ‘You mentioned you had felt…’

HISTORY OF PRESENTING COMPLAINT

⦁ Interrogate the patient further about the presenting complaint
⦁ A useful guide, e.g. for pain, is the mnemonic ‘SOCRATES’:
• Site
• Onset
• Character
• Radiation
• Alleviating factors
• Timing
• Exacerbating factors
• Severity (scale 1–10)
• And associated Symptoms

PAST MEDICAL HISTORY

⦁ Enquire about diseases relating to the presenting complaint. For example, for chest
pain:
• Coronary heart disease/angina/myocardial infarction (MI)
• Indigestion/reflux/hiatus hernia
• Asthma/chronic obstructive pulmonary disease (COPD)/pulmonary fibrosis
• Deep vein thrombosis/pulmonary embolism/hypercoagulability
⦁ Ask all patients if they have a history of important diseases (mnemonic ‘JAM
THREADS Ca’):
• Jaundice
• Anaemia and other haematological conditions
• Myocardial infarction
• Tuberculosis
• Hypertension and heart disease
• Rheumatic fever
• Epilepsy
• Asthma and chronic obstructive pulmonary disease (COPD)
• Diabetes
• Stroke
• Cancer

DRUG HISTORY
⦁ Enquire about all medications including creams, drops, the oral contraceptive and
herbal/vitamin preparations

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 H i s t o r y t a k i n g s k i l l s     3

⦁ Specify:
• Route
• Dose
• Frequency
• Compliance
⦁ Take a detailed allergy history, e.g. which medications/foods and the symptoms

FAMILY HISTORY
⦁ Ask the patient about any relevant family diseases, e.g. coronary heart disease, diabetes
⦁ Enquire about the patient’s parents, and the cause and age at death if deceased
⦁ Sketch a short family tree, including any offspring (see Fig. 1.1)

Key:

Male

Female

Deceased

Disease sufferer
e.g. haemophilia

Married

Offspring

Figure 1.1 Example family tree

SOCIAL (AND PSYCHIATRIC) HISTORY

⦁ Assess any alcohol use in approximate units/week
⦁ Ask about tobacco use – quantify with ‘pack years’ (number of packets of 20 cigarettes
smoked per day multiplied by number of years smoking)
⦁ Employment history, current and past, including exposure to pathogens, e.g. asbestos
⦁ Enquire about home situation, including any pets
⦁ Enquire about any history of psychiatric disease

SYSTEMS REVIEW
⦁ Run through a comprehensive list of symptoms from all systems:
• Cardiovascular, e.g. chest pain, palpitations
• Respiratory, e.g. cough, dyspnoea
• Gastrointestinal, e.g. abdominal pain, diarrhoea
• Genitourinary, e.g. dysuria, discharge
• Neurological, e.g. numbness, weakness
• Musculoskeletal, e.g. aches, pains
• Psychiatric, e.g. depression, anxiety

SUMMARY
⦁ Provide a short summary of the history including:

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 4    H i s t o r y

• Name and age of patient

• Presenting complaint
• Relevant medical history
⦁ Give a differential diagnosis (e.g. ‘This could be a myocardial infarction or
oesophageal spasm’)
⦁ Formulate a short investigation and treatment plan

CHEST PAIN
INTRODUCTION
⦁ Introduce yourself
⦁ Confirm the patient’s name
⦁ Confirm the reason for meeting
⦁ Adopt appropriate body language

HISTORY OF PRESENTING COMPLAINT

The mnemonic ‘SOCRATES’ is useful for assessing chest pain (see p. 2). Enquire about:
⦁ Site – central or left chest, retrosternal, epigastric
⦁ Onset – sudden, gradual, related to trauma/exertion
⦁ Character – crushing, heavy, tight band, pleuritic, burning
⦁ Radiation – radiating to left arm, neck, jaw or back
⦁ Alleviation – rest, glyceryl trinitrate (GTN) spray, sitting forward (pericarditis)
⦁ Timing – related to exertion or occurring at rest
⦁ Exacerbating factors – effort, emotion, movement, food, respiration, cold weather
⦁ Severity (scale 1–10)
⦁ And associated Symptoms:
• Dyspnoea, palpitations
• Syncope/collapse
• Sweating, burping, nausea/vomiting
• Ankle swelling
• Calf swelling
• Paroxysmal nocturnal dyspnoea (PND) or orthopnoea
• Cough, haemoptysis, sputum
• Fever, constitutional upset, coryza
• Panic attacks, anxiety

PAST MEDICAL HISTORY

⦁ Vascular disease:
• Angina, previous MI, previous angioplasty or coronary artery bypass graft
(CABG) surgery
• Claudication
• Cerebrovascular disease, transient ischaemic attacks
• Risk factors:
♦ Hypertension
♦ Hyperlipidaemia

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 S h o r t n e s s o f b r e a t h     5

♦ Diabetes
♦ Smoking
♦ Family history (MI <60 years of age, hyperlipidaemia)
⦁ Thromboembolic disease:
• Recent surgery, cancer, immobility
• Inherited hypercoagulable state, e.g. protein S or C deficiency
• Oral contraceptive/hormone replacement therapy
• Smoking
⦁ Pneumothorax:
• Tall, thin man
• Connective tissue disease (e.g. Marfan’s)

DRUG HISTORY
⦁ Cardiac medications: β-blockers, diuretics, antiplatelet agents, GTN spray
⦁ Recreational drug use, e.g. cocaine (coronary artery spasm)
⦁ Chronic non-steroidal anti-inflammatory drug (NSAID) use causing gastritis/
oesophagitis/reflux

SOCIAL HISTORY
⦁ Smoking
⦁ Alcohol intake
⦁ Diet (fatty food, salt intake)
⦁ Lifestyle, exercise
⦁ Recent immobility/major surgery/long-haul travel

BOX 1.2 DIFFERENTIAL DIAGNOSIS: CHEST PAIN

Cardiovascular: Respiratory:
⦁⦁ MI ⦁⦁ Pulmonary embolism
⦁⦁ Acute coronary syndrome (non-ST ⦁⦁ Pneumonia
elevation MI, unstable angina) ⦁⦁ Pneumothorax
⦁⦁ Angina (induced by effort and Musculoskeletal:
relieved by rest) ⦁⦁ Costochondritis (Tietze’s syndrome)
⦁⦁ Acute aortic dissection ⦁⦁ Chest wall injuries
⦁⦁ Pericarditis
Psychosomatic:
Gastrointestinal: ⦁⦁ Anxiety/depression
⦁⦁ Reflux oesophagitis
⦁⦁ Oesophageal spasm
⦁⦁ Peptic ulcer disease

SHORTNESS OF BREATH
INTRODUCTION
⦁ Introduce yourself
⦁ Confirm the patient’s name

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 6    H i s t o r y

⦁ Confirm the reason for meeting

⦁ Adopt appropriate body language

HISTORY OF PRESENTING COMPLAINT

Enquire about:
⦁ Onset and duration – acute, chronic, constant, intermittent
⦁ Exacerbating factors – effort, emotion, movement, cold weather
⦁ Alleviation – rest, inhalers
⦁ Timing – related to exertion
⦁ Associated symptoms:
• Wheeze
• Stridor
• Cough – productive or dry, colour/viscosity of sputum
• Fever, night sweats or weight loss
• Haemoptysis – how much: teaspoon, cup-full
• Chest pain – pleuritic, cardiac
• Palpitations
• Nausea and vomiting, sweating, dizziness
• Ankle swelling
• PND
• Orthopnoea – number of pillows
• Exercise tolerance – quantify, e.g. number of stairs, distance on the flat

PAST MEDICAL HISTORY

⦁ Asthma: frequency of attacks, admissions to hospital or intensive care unit
⦁ COPD: frequency of exacerbations, admissions (as for asthma), use of home oxygen
(number of hours) and home nebulizers
⦁ Recurrent lower respiratory tract infections
⦁ Cardiac failure or structural disease
⦁ Arrhythmias
⦁ Deep vein thrombosis, procoagulant states (e.g. pregnancy, cancer, surgery)

DRUG HISTORY
⦁ Nebulizers
⦁ Cardiac medications
⦁ Diuretics, e.g. furosemide
⦁ Angiotensin-converting enzyme inhibitors

FAMILY HISTORY
⦁ History of atopy – asthma, eczema, hay fever
⦁ Tuberculosis

SOCIAL HISTORY
⦁ Smoking history (active and passive)
⦁ Occupation and exposure to coal, dust, asbestos

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 Fe v e r / p y r e x i a o f u n k n o w n o r i g i n     7

⦁ Animal exposure (pets, farming)

⦁ Tuberculosis exposure
⦁ Limitation of daily activities by shortness of breath

BOX 1.3 DIFFERENTIAL DIAGNOSIS

Acute: Chronic:
⦁⦁ Asthma ⦁⦁ COPD
⦁⦁ Acute exacerbation of COPD ⦁⦁ Cardiac failure
⦁⦁ Lower respiratory tract infection ⦁⦁ Pulmonary fibrosis
⦁⦁ Pulmonary oedema ⦁⦁ Anaemia
⦁⦁ Pulmonary embolism ⦁⦁ Arrhythmias
⦁⦁ Pneumothorax ⦁⦁ Cystic fibrosis
⦁⦁ Pleural effusion ⦁⦁ Pulmonary hypertension
⦁⦁ Lung cancer
⦁⦁ Anxiety/panic attack
⦁⦁ Metabolic acidosis

FEVER/PYREXIA OF UNKNOWN ORIGIN

INTRODUCTION
⦁ Introduce yourself
⦁ Confirm the patient’s name
⦁ Confirm the reason for meeting
⦁ Adopt appropriate body language

HISTORY OF PRESENTING COMPLAINT

⦁ Onset – sudden, gradual
⦁ Character – constant, intermittent
⦁ Frequency of peaks in temperature
• Has the temperature been recorded?
⦁ Alleviation – rest, paracetamol
⦁ Timing – related to exertion
⦁ Exacerbating factors – climate/weather, time of day
⦁ Associated symptoms/signs:
• Rigors or shivering
• Sweating (especially at night)
• Weight loss
• Anorexia
• Feeling faint or dizziness, syncopal episodes
• Fatigue
• Lumps, tender lymph nodes
• Pain
• Cough and sputum (lower respiratory tract infection)
• Diarrhoea and vomiting, abdominal pain (gastroenteritis)

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 8    H i s t o r y

• Urinary frequency, dysuria, haematuria (urinary tract infection [UTI])

• Rashes or skin changes, areas of erythema (viral illnesses, cellulitis)
• Headache, neck stiffness, photophobia (meningitis)
• Heart failure, track marks, lethargy, rash, new murmur (infective endocarditis)

PAST MEDICAL HISTORY

⦁ Recent surgery
⦁ Recent illness, e.g. upper respiratory tract infection
⦁ Blood transfusions

DRUG HISTORY
⦁ Intravenous drug use
⦁ Appropriate malaria prophylaxis when travelling and compliance
⦁ Immunizations up to date

FAMILY HISTORY
⦁ Any family members with contagious disease
⦁ Animal – contact, bites

SEXUAL HISTORY
⦁ Sexual history – recent sexual practices (see p. 205)

TRAVEL HISTORY
⦁ Travel history – location, appropriate vaccinations, diet, food hygiene, swimming

SOCIAL HISTORY
⦁ Tattoos
⦁ Piercings
⦁ Occupational exposure, e.g. to animals

BOX 1.4 COMMON DIFFERENTIAL DIAGNOSES OF PYREXIA OF UNKNOWN ORIGIN

Infective:
⦁⦁ Bacterial: e.g. pneumonia, UTI, meningitis, endocarditis, abdominal/pelvic
abscess
⦁⦁ Viral: e.g. gastroenteritis, hepatitis, human immunodeficiency virus (HIV)
seroconversion
⦁⦁ Parasitic: e.g. malaria, schistosomiasis
Inflammatory: e.g. systemic lupus erythematosus, rheumatoid arthritis, Crohn’s
disease
Malignancy: e.g. lymphoma, leukaemia, hepatocellular carcinoma
Others: e.g. pulmonary embolus, factitious, recent vaccination, thyrotoxicosis

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 A b d o m i n a l p a i n     9

INVESTIGATIONS
There are numerous investigations, depending on the history, including:
⦁ Full blood count, urea and electrolytes, liver function tests, C-reactive protein,
erythrocyte sedimentation rate, thyroid function tests
⦁ Viral screen, e.g. Epstein–Barr virus, cytomegalovirus, HIV
⦁ Autoimmune screen, e.g. antinuclear antibody, antineutrophil cytoplasmic antibody
⦁ Blood cultures
⦁ Blood film to exclude malaria and haematological disorders
⦁ Sputum culture
⦁ Mid-stream urinalysis
⦁ Stool culture
⦁ Chest X-ray
⦁ Electrocardiogram
For difficult cases, echocardiography (endocarditis), computed tomography and positron
emission tomography can help localize abnormalities giving rise to the fever. Referral to a
genitourinary medicine clinic or a tropical disease specialist may be warranted if indicated
by the history.

ABDOMINAL PAIN
INTRODUCTION
⦁ Introduce yourself
⦁ Confirm the patient’s name
⦁ Confirm the reason for meeting
⦁ Adopt appropriate body language

HISTORY OF PRESENTING COMPLAINT

Enquire about:
⦁ Site – where did it start and has it moved?
⦁ Onset – sudden, gradual
⦁ Character – crampy, colicky, sharp, burning
⦁ Radiation – e.g. loin to groin (renal colic)
⦁ Alleviation – relieved by opening bowels or vomiting?
⦁ Timing – related to eating/bowels/micturition/menstruation/movement?
⦁ Exacerbating factors
⦁ Severity (scale 1–10), does it wake you?
⦁ And associated Symptoms:
• Nausea and vomiting – haematemesis, ‘coffee-ground’ vomit, bile-stained or
feculent?
• Dysphagia
• Dyspepsia
• Change in bowel habit – e.g. diarrhoea/constipation, altered frequency, colour,
consistency, pale, offensive smell, frothy, hard to flush away (steatorrhoea), blood

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 10    H i s t o r y

or mucus present
• Rectal bleeding
• Bloating, flatulence
• Weight gain/loss
• Appetite change
• Jaundice, pruritus, dark urine, pale stools
• Rigors/fever

Right Epigastric Left Right Left

hypochondrium region hypochondrium upper upper
quadrant quadrant
Right Umbilical Left
lumbar region region lumbar region
Right Left
lower lower
Right Supra- Left
quadrant quadrant
iliac fossa pubic iliac fossa
region

(a) (b)

• Haematuria, dysuria, vaginal discharge or bleeding

Figure 1.2 Areas of the abdomen: (a) ninths or (b) quadrants

PAST MEDICAL HISTORY

⦁ Inflammatory bowel disease – Crohn’s disease, ulcerative colitis
⦁ Diverticular disease
⦁ Previous abdominal/pelvic surgery (adhesions causing bowel obstruction)
⦁ Recent trauma or injury (e.g. splenic rupture)
⦁ Menstruation (pregnant/ectopic) and sexual history (pelvic inflammatory disease)
⦁ Other common diseases: MJ THREADS Ca (see p. 2)

DRUG HISTORY
⦁ NSAIDs
⦁ Laxatives
⦁ Opiates
⦁ Antibiotics, e.g. erythromycin

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 A b d o m i n a l p a i n     11

FAMILY HISTORY
⦁ Inflammatory bowel disease
⦁ Polyps, bowel cancer
⦁ Jaundice
⦁ Family members with diarrhoea and vomiting

SOCIAL HISTORY
⦁ Alcohol intake
⦁ Recreational drug use
⦁ Travel abroad
⦁ Recent potentially infected food intake
⦁ Blood transfusions, tattoos
⦁ Sexual history (see p. 205)

BOX 1.5 DIFFERENTIAL DIAGNOSIS OF ABDOMINAL PAIN

Gastrointestinal: Splenic:
⦁⦁ Gastritis, dyspepsia, peptic ulcer ⦁⦁ Infarction
disease ⦁⦁ Rupture
⦁⦁ Appendicitis Genitourinary:
⦁⦁ Peritonitis ⦁⦁ Acute pyelonephritis
⦁⦁ Perforated gastric ulcer ⦁⦁ Renal colic
⦁⦁ Bowel obstruction ⦁⦁ Cystitis/UTI
⦁⦁ Diverticulitis ⦁⦁ Ectopic pregnancy
⦁⦁ Gastroenteritis ⦁⦁ Torsion or rupture of ovarian cyst
⦁⦁ Inflammatory bowel disease ⦁⦁ Pelvic inflammatory disease
⦁⦁ Mesenteric adenitis ⦁⦁ Salpingitis
⦁⦁ Strangulated hernia ⦁⦁ Endometriosis
⦁⦁ Volvulus ⦁⦁ Fibroids
⦁⦁ Intussusception ⦁⦁ Dysmenorrhoea
⦁⦁ Irritable bowel syndrome ⦁⦁ Referred pain of testicular torsion
⦁⦁ Pancreatitis
Other:
⦁⦁ Malignancy
⦁⦁ Abdominal aortic aneurysm
Hepatobiliary: ⦁⦁ Mesenteric thrombosis or embolus
⦁⦁ Cholangitis ⦁⦁ Diabetic ketoacidosis
⦁⦁ Acute cholecystitis ⦁⦁ Sickle cell crisis
⦁⦁ Cholelithiasis (gall stones) ⦁⦁ Acute porphyria
⦁⦁ Hepatitis ⦁⦁ Acute MI
⦁⦁ Fitz-Hugh–Curtis syndrome
(chlamydial perihepatitis)

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 12    H i s t o r y

CHANGE IN BOWEL HABIT/RECTAL BLEEDING

INTRODUCTION
⦁ Introduce yourself
⦁ Confirm the patient’s name
⦁ Confirm the reason for meeting
⦁ Adopt appropriate body language

HISTORY OF PRESENTING COMPLAINT

Enquire about:
⦁ Normal bowel habit (for the patient)
⦁ Changes:
• Symptoms:
♦ Frequency of bowel opening
♦ Constipation
♦ Diarrhoea – watery, loose
♦ Steatorrhoea – pale, offensive smell, frothy, hard to flush away
♦ Rectal blood – mixed in, on paper, in toilet pan, altered or frank blood
♦ Any pus, slime or mucus
• Onset – sudden, gradual
• Duration
• Timing – any relation to food, menstruation, activity level, time of day
• Alleviating factors – e.g. certain food avoidance
• Exacerbating factors – e.g. exercise, sleep patterns, food
• Associated symptoms:
♦ Nausea and vomiting – haematemesis, ‘coffee grounds’, bile-stained or
faeculent
♦ Dysphagia
♦ Dyspepsia
♦ Bloating, flatulence
♦ Weight gain/loss
♦ Appetite change, diet change
♦ Jaundice, pruritus, dark urine, pale stools
♦ Rigors/fever
♦ Haematuria, dysuria, vaginal discharge

PAST MEDICAL HISTORY

⦁ Inflammatory bowel disease – Crohn’s disease, ulcerative colitis
⦁ Coeliac disease
⦁ Diverticular disease
⦁ Groin/midline/incisional hernias
⦁ Previous abdominal surgery (e.g. adhesions causing bowel obstruction)
⦁ Metabolic disturbances, e.g. thyroid disease

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 Ti r e d n e s s     13

DRUG HISTORY
⦁ NSAIDs
⦁ Laxatives
⦁ Opiates
⦁ Antibiotics, e.g. erythromycin

FAMILY HISTORY
⦁ Inflammatory bowel disease
⦁ Polyps, bowel cancer
⦁ Family members with diarrhoea and vomiting

SOCIAL HISTORY
⦁ Alcohol intake
⦁ Recreational drug use
⦁ Travel abroad
⦁ Recent potentially infected food intake
⦁ Sexual history (see p. 205)

BOX 1.6 DIFFERENTIAL DIAGNOSIS OF CHANGE IN BOWEL HABIT

Gastrointestinal: Infective:
⦁⦁ Appendicitis ⦁⦁ Bacterial, e.g. Salmonella species
⦁⦁ Peritonitis ⦁⦁ Viral
⦁⦁ Perforated gastric ulcer ⦁⦁ Fungal
⦁⦁ Bowel obstruction ⦁⦁ Protozoan
⦁⦁ Ileus, e.g. postoperative Drugs:
⦁⦁ Diverticulitis ⦁⦁ Opiates
⦁⦁ Gastroenteritis ⦁⦁ Laxatives
⦁⦁ Inflammatory bowel disease (Crohn’s ⦁⦁ Antibiotics
disease or ulcerative colitis) ⦁⦁ Tricyclic antidepressants
⦁⦁ Strangulated hernia
Metabolic:
⦁⦁ Volvulus
⦁⦁ Thyroid disease
⦁⦁ Intussusception
⦁⦁ Diabetes (autonomic disease)
⦁⦁ Irritable bowel syndrome
⦁⦁ Carcinoid
⦁⦁ Pancreatitis
⦁⦁ Malignancy Others:
⦁⦁ Biliary obstruction, e.g. gallstones ⦁⦁ Anxiety
⦁⦁ Anal pain, e.g. fissure, fistula ⦁⦁ Depression
⦁⦁ Diet

TIREDNESS
INTRODUCTION
⦁ Introduce yourself
⦁ Confirm the patient’s name

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 14    H i s t o r y

⦁ Confirm the reason for meeting

⦁ Adopt appropriate body language

HISTORY OF PRESENTING COMPLAINT

Enquire about:
⦁ Onset and duration:
• Sudden onset and short history, e.g. post-viral cause
• Long duration (more suggestive of emotional origin)
⦁ Related factors:
• If related to exertion – more likely organic cause
• Time of day, e.g. rheumatoid arthritis worse on waking
• Improved after rest, e.g. myasthenia gravis
⦁ Associated symptoms:
• Weight loss, anorexia, dyspnoea – suggest underlying pathology, e.g. cancer
• Weight gain, constipation, dry skin and hair, cold intolerance – e.g.
hypothyroidism
• Chronic pain
• Rectal bleeding, abdominal pain, menorrhagia – e.g. anaemia
⦁ Sleep patterns:
• Early morning waking – depression
• Snoring, daytime somnolence, early morning headaches, obesity – obstructive
sleep apnoea (OSA) (see Box 1.7)

PAST MEDICAL HISTORY

⦁ Recent viral illnesses
⦁ Sleep apnoea
⦁ Cardiac disease
⦁ Hypothyroidism (or previous thyroid-related treatment including surgery)
⦁ Endocrine diseases including diabetes mellitus
⦁ Renal failure
⦁ Recent stress or life event. Psychiatric problems

BOX 1.7 EPWORTH SLEEPINESS SCALE – ESTABLISHES POSSIBLE DIAGNOSIS OF OSA

For each question score for chance of dozing (0 = no chance, 1 = slight, 2 =

moderate, 3 = high; score >11/24 significant)
Likelihood of falling asleep when:
⦁⦁ Sitting and reading
⦁⦁ Watching television
⦁⦁ Sitting inactive in a public place
⦁⦁ Passenger in a car for 1 hour
⦁⦁ Lying down to rest in the afternoon
⦁⦁ Sitting and talking to someone
⦁⦁ Sitting quietly after lunch (without alcohol)
⦁⦁ Sitting in the car in traffic for few minutes

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Another random document with
no related content on Scribd:
know, there is no proof that it possesses any virtue in meningeal
tuberculosis. It has the high authority of Charles West,14 however,
who thinks the remedy is more encouraging than any other, and who
mentions one instance in which recovery took place under its
employment. He recommends that two grains be given every four
hours to a child three years old, the bowels being kept free. Most
authorities recommend much higher doses, such as ten or fifteen
grains, three or four times daily.
14 Op. cit., p. 102.

Counter-irritation to the head or back of the neck was formerly much

employed, but is now generally abandoned, as giving rise to much
discomfort without obvious beneficial effect. In the cases reported by
Hahn, already alluded to under the head of Prognosis, recovery is
attributed to the energetic application of tartar-emetic ointment to the
scalp, producing extensive ulceration, which in one of them lasted
more than ten months before cicatrization took place. A careful
examination of the reports of these cases satisfies me that but two
out of the seven were really examples of tubercular meningitis. How
far the recovery in the successful cases is to be attributed to the
treatment is very doubtful. Small blisters applied to the vertex or
back of the neck are alluded to favorably by West, but he quotes no
observations in which they were followed by benefit.

Tubercular Meningitis in the Adult.

Tubercular meningitis may occur at any age, but after the period of
childhood it is most frequent between the ages of sixteen and thirty
years. About 75 per cent. of the patients are males, and 25 per cent.
females.15 The disease does not differ essentially in its course and
symptoms from that in children. A family history of tuberculosis is
common, or the patient may be already suffering from phthisis,
scrofulous glands, cheesy deposits in various organs, caries of the
bone, syphilis, or other constitutional affections. According to Seitz,
in 93.5 per cent. out of 130 cases with autopsies chronic
inflammatory conditions or caseous deposits were found in various
organs of the body. Many cases are examples of acute tuberculosis
in which the brunt of the disease has fallen upon the brain rather
than the other organs.
15 Seitz, op. cit., p. 9.

When cerebral symptoms supervene upon acute disease, such as

typhoid fever, pericarditis, acute rheumatism, pneumonia, the
exanthemata, etc., the diagnosis between tubercular and simple
meningitis is important, because the latter is not necessarily fatal,
while the former is almost never recovered from. If the patient were
previously healthy and presumably free from tubercular disease, the
chances would be in favor of the simple form. A rapid course of the
disease would also speak for acute meningitis, and recovery would
almost certainly preclude tubercular meningitis. In some cases the
diagnosis is difficult or impossible in the beginning.

In cases beginning without acute antecedents—in adults as in

children—there is no pathognomonic symptom, but the combination
and succession of the phenomena are usually sufficient for the
diagnosis. Headache, depression or irritability of temper, delirium,
half-closed eyes, ptosis of one lid, squinting, inequality and
sluggishness of the pupils, moderate fever, sunken belly, vomiting,
constipation, slow and irregular pulse, sopor gradually deepening to
coma, with occasional convulsions or paralysis of the limbs, followed
in the course of two or three weeks by death, especially if occurring
in a patient who has already presented signs of tuberculosis in other
organs, point almost unmistakably to tubercular meningitis. Some of
the symptoms may not be strongly pronounced, one or two may be
absent, but the general picture will suggest no other disease.
According to Seitz, tubercle of the choroid is rare in tubercular
meningitis of the adult. It is usually associated with tuberculosis of
other organs, the pia being free. The subjoined cases are
illustrations of the disease in adolescence and adult life:
Case I.—A lad sixteen years old, always somewhat delicate, with a
cough and morning expectoration of some months' standing, exerted
himself immoderately in gymnastic exercise on the afternoon of
Sept. 24, 1875. That night he was awakened by cough and
hæmoptysis. Signs of consolidation were found at the apices of both
lungs. In three months there were swelling, induration, and
suppuration of one testicle. Some months later, pain in the right arm,
stiffness of the shoulder-joint, and an abscess communicating with
the joint, from which small spicula of bone were discharged. He was
about, and even attended school, for more than a year from the time
of the attack of hæmoptysis. About Jan. 1, 1877, he began to
complain of severe pain in the forehead, with nausea (but no
vomiting) and constipation. Jan. 27th he took to his bed, complaining
chiefly of pain in the forehead and eyes. Feb. 1st he was drowsy,
irritable, and delirious. Feb. 3d incontinence of urine and constant
delirium. Up to this time the pulse had not been above 76 in the
minute, and on this day it was 64. The next day, Feb. 4th, he was
wholly unconscious; pulse 96, pupils dilated. Feb. 5th, left hand in
constant motion; pulse 112. From this time the pulse steadily
increased in frequency. Feb. 6th he swallowed food, notwithstanding
his stupor. Feb. 7th he answered questions; there was oscillation of
the eyeballs, and epistaxis from constant picking of the nose. He
died Feb. 9th, the pulse being 144 and the respirations 60 in the
minute for several hours previous. The temperature never rose
above 101.7° F. There was never any vomiting. The duration of the
case was thirteen days, in addition to the prodromic period of twenty-
seven days.—Autopsy by R. H. Fitz: The pia of the base of the brain
from the medulla to the optic thalamus contained a large number of
gray miliary tubercles, old and recent, and the same condition was
found in the surfaces of the fissure of Sylvius. Ventricles distended
with fluid, ependyma thick and translucent. A moderate-sized cavity
in the apex of the left lung, with cheesy contents. Both lungs
contained an abundance of hard, gray, miliary tubercles. Left kidney
contained a wedge-shaped, cheesy mass of the size of a walnut,
with numerous tubercles. Left testicle contained a cheesy mass of
the size of a walnut; both epididymes were cheesy. The mucous
membrane of the bladder contained tubercles near the neck. The
vesiculæ seminales contained softened cheesy masses with
openings into the urethra. There was a fistulous opening into the
right shoulder-joint.

Case II.—Emeline K. L——, 32 years old, single, nurse, had become

much exhausted by taking care of a difficult case, and entered
Massachusetts General Hospital March 6, 1883, complaining since
four days of a little cough, slight expectoration, and chilliness, but no
rigor. She seemed hysterical. There was complaint of severe pain in
the head, chest, and abdomen. A slight systolic murmur was found
at the apex of the heart, and a few moist râles at the base of the
chest on both sides behind. The urine was normal. Temperature,
103° F. Three weeks after entrance she began to be delirious,
especially at night. April 13th, five weeks and three days after
entrance, she was semi-conscious, but would put out her tongue and
open her eyes when requested to do so; the abdomen was
distended, the pupils were dilated and unequal; there was twitching
of the muscles of the right side of the face. Careful examination only
disclosed occasional fine râle at the base of right chest. She died
April 16th, having been completely unconscious for twenty-four
hours. There was no vomiting throughout the case. The temperature
was very irregular, ranging between 100° and 103° F., and once as
high as 104° F.; it was usually one or two degrees higher at night
than in the morning. Pulse, generally from 100 to 110; it rose steadily
during the last few days to 160 at the time of death.—Autopsy: Pia
mater of brain œdematous, slightly opaque; its lower surface,
especially at the base of the brain, showed numerous minute gray
tubercles; enlarged cheesy glands at the base of the neck; small,
opaque, gray tubercles scattered rather sparsely throughout both
lungs. There was also miliary tuberculosis of the liver, spleen, and
kidneys.
CHRONIC HYDROCEPHALUS.
 BY FRANCIS MINOT, M.D.

SYNONYMS.—Dropsy of the brain, Dropsy of the head.

DEFINITION.—A gradual accumulation of serous fluid in the brain,

occupying either the ventricles or the cavity of the arachnoid, or both,
occurring chiefly in infants or very young children.

The term hydrocephalus, which was applied by the older writers to

accumulations of serous fluid both within and also without the
cranium, termed distinctively internal and external hydrocephalus, is
now restricted to dropsical effusions either between the meninges or
within the ventricular cavities. These may be acute or chronic, and
they arise from the same conditions which are followed by the
effusion of serum in other parts of the body; that is to say, from an
alteration in the serous membrane lining a cavity, from an obstruction
in the capillary circulation with increased tension in the larger
vessels, from an altered condition of the blood, etc.

Chronic hydrocephalus is almost entirely confined to young children,

and is probably due to an arrested development of the brain, as
shown by its being usually congenital, by the dwarfed intellectual
condition of the patient, and by its frequent association with spina
bifida. The pathogeny of the disease is, however, still obscure.
Whether the abnormal accumulation of serous fluid is to be ascribed
to a chronic alteration of the ventricular walls or of the choroid
plexuses, allied to inflammation, such as occurs in the pleura, for
example, causing an increased secretion, or to a closure of the
communication between the ventricles and the spinal cavity, as
suggested by the late John Hilton, resulting in dropsy by retention, or
to some other cause, is not yet determined. Hilton says:1 “In almost
every case of internal hydrocephalus which I have examined after
death I found that this cerebro-spinal opening [between the fourth
ventricle and the spinal canal] was so completely closed that no
cerebro-spinal fluid could escape from the interior of the brain; and,
as the fluid was being constantly secreted, it necessarily
accumulated there, and the occlusion formed, to my mind, the
essential pathological element of internal hydrocephalus.” Sieveking,
commenting upon Hilton's theory, says:2 “While giving these facts
due weight, it must be pointed out that we are yet far from
understanding either how the fluid is poured into the cerebral cavities
or how it is removed, and that we do not positively know that the
spinal canal has any better means of getting rid of an excess of fluid
than the cerebral cavities have.” An arrest of the growth of the brain
is supposed by some pathologists to account for ventricular as well
as arachnoidal dropsy by the creation of a vacuum in the cavity of
the cranium, which is filled by exudation of the more fluid portion of
the blood from the vessels or of lymph from the lymphatics.
1 John Hilton, Lectures on Rest and Pain, etc., 2d ed., New York, 1879, p. 22.

2 Jones and Sieveking's Pathological Anatomy, 2d ed., London, 1875, p. 248.

ETIOLOGY.—That chronic hydrocephalus in young children is in a

large proportion of cases an hereditary disease is shown by the fact
that it is frequently congenital, that more than one child in a family is
occasionally affected by it, and that while one child is hydrocephalic
others may be idiotic. A scrofulous taint in the family history is
noticeable in many cases, the evil effect of which is frequently
enhanced by unfavorable sanitary conditions of life, especially by
residence in dark, damp, ill-ventilated, and badly-drained apartments
and by insufficient or unwholesome food. Hence the disease is more
frequently met with among the poor than in the well-to-do classes of
society. There is a difference of opinion as to whether it ever arises
in consequence of external violence, such as a blow on the head, or
of some strong impression, like fright or grief, acting on the mother of
the child during pregnancy. The probability is that such causes would
not be efficient except in cases where a predisposition to
hydrocephalus had already existed. West3 mentions the case of a
healthy child five months old who fell out of the arms of her nurse,
and was taken with a fit the same day. She apparently recovered,
but when a year old had frequent returns of convulsions. At the age
of fifteen months the head began to enlarge, and it continued to
increase in size until she was three years old, when she was
attacked by measles, and died in a few days with convulsions and
coma. The symptoms, both bodily and mental, were typical of
hydrocephalus, and the diagnosis was fully confirmed by the
autopsy.
3 Op. cit., p. 127.

The causes of chronic hydrocephalus in older subjects and in adults

are, in addition to the above mentioned, chiefly mechanical. Any
lesion which hinders the exit of venous blood from the cranium may
be followed by dropsy of the arachnoid cavity or ventricles. The
principal ones are tumors of the brain or its membranes, the effusion
of lymph in the neighborhood of veins, thrombosis of the cerebral
sinuses, compression of numerous small vessels by tubercular
granulations, obstructions outside the cranium, including tumors of
the neck, aneurisms, obstructive disease of the heart, emphysema
and cirrhosis of the lungs, besides diseases giving rise to general
dropsy, as the different forms of nephritis, marasmus, the various
cachexiæ, etc.

SYMPTOMS.—When the disease is already somewhat advanced

before birth, the head is often abnormally large, the cranial bones
are separated, the fontanels are distended and fluctuating, and it
occasionally happens that delivery of the distended head can only be
effected after the fluid has been evacuated by puncture. Even when
there is no abnormal increase in the size of the head, indications of
cerebral disturbance are sometimes apparent from birth, such as
strabismus or convulsions recurring with more or less frequency,
along with signs of failure of the general health. In the course of
some weeks, or, it may be, months, the attention of the parents is
attracted to the prominence of the child's forehead, strongly
contrasting with the comparatively diminutive size of the face. Soon
an enlargement of the fontanels is perceived, the sutures between
the cranial bones become broader, and the head assumes a globular
shape from the pressure of the contained fluid. The separation of the
bones at the vertex of the skull causes the os frontis to protrude
forward, the parietals backward and outward, and the occipital
backward and downward. The orbital plates of the frontal bone yield
to the pressure of the fluid behind them, and from a horizontal
position tend to assume a vertical one, protruding the eyeballs,
which have a peculiar downward direction. The sclerotica is visible
above the iris, and the latter is partially covered by the lower eyelid.
The enlargement of the head is progressive, though not uniformly so,
there being pauses of weeks or months during which it is arrested. If
it be considerable, the cranial bones are usually thinned, so that the
skull becomes translucent when opposite a bright light. When there
is a wide separation of the bones there is an unusual development of
ossa triquetra in the sutures.

In cases in which the ossification of the cranium is considerably

advanced before the beginning of the disease, the enlargement of
the head is apt to be correspondingly less. If all the sutures are
consolidated, there may be no increase in size, and this is especially
true of the mechanical dropsy of adult life. The dropsical effusion,
which is then moderate in amount, finds room through compression
of the brain-substance, and part of it escapes into the spinal canal.

The size of the hydrocephalic head varies considerably. Where there

has been an early arrest of the disease it may be but slightly above
the normal. On the other hand, the dimensions are sometimes
enormous. In the Warren Museum of Harvard University is a cranium
which measures 27½ inches in its greatest circumference, and 20½
inches from one auditory foramen to the other over the top of the
head. Its internal capacity is 257 cubic inches. The patient, who died
at the age of three years, was never able to sit up and support the
head, or even to turn it from the left side, on which she continually
lay; she never spoke, and seemed to have no intelligence. The skull
of the celebrated James Cardinal measured 32¼ inches in its largest
circumference.4 Even more remarkable instances are on record. The
dimensions of the fontanels, particularly the anterior, usually
correspond with those of the skull in general. During any strong
muscular effort on the part of the patient the membrane covering
them is seen to be bulged out by pressure from the fluid beneath.
The enlargement is not always uniform; it may be in part or wholly
confined to one side, owing to consolidation of the sutures of the
opposite side, or because only one of the lateral ventricles is
affected. The scalp is traversed by numerous distended veins. The
hair is very scanty. The head has a soft, fluctuating feel, and the
walls sometimes seem to crackle beneath the fingers, like
parchment.
4 Reports of Medical Cases, etc., by Richard Bright, M.D., London, 1831, vol. i. p.
431.

In cases of moderate severity there may be few or no symptoms of

active cerebral disturbance, such as convulsions or paralysis, but the
child does not learn to talk, to walk, or to control the sphincters even
at the age of three or four years, and the signs of imperfect mental
development are evident. He is apt to be irritable or mischievous,
and even when not actually idiotic is very backward in evincing signs
of intelligence. There are, however, not a few exceptions to this, and
some children with large hydrocephalic heads are intelligent and
amiable. The cranium of a girl who died at the age of sixteen years is
preserved in the Warren Museum. It measures 24¼ inches in
circumference and 17¼ inches from one auditory meatus to the
other over the vertex, and the bone is in no place more than one-
eighth of an inch in thickness. The child was an inmate of a house of
industry, where she was instructed in the usual branches of
knowledge taught in our common schools, until at length, such was
her capacity, she was entrusted with the teaching of the other pauper
children, and she had an excellent character for intelligence and
moral worth. She died of phthisis. On post-mortem examination “the
brain was found floating, as it were, in a large collection of water.” As
in other chronic diseases, there are often pauses, from time to time,
of variable duration, in which there is some improvement in the
condition of the patient, as well as a temporary arrest in the
enlargement of the head. The growth of the child in stature is often
retarded, and when life is prolonged the individual is more or less
dwarfed. In some cases there is a considerable increase in the
amount of adipose tissue, and the appetite is often voracious. L.
Fürst reports5 the case of a hydrocephalic girl, sixteen years old,
whose height (or, rather, length, for she was unable to stand) was 81
centimeters (nearly 32 inches), corresponding to the stature of a
child between three and four years old. The periphery of the head
measured 511/5 centimeters (20¼ inches). The anterior fontanel was
still open. The age was verified by reference to the registry of birth at
the police-office.
5 “Exquisite Wachsthumshemmung bei Hydrocephalus chronicus,” von Dr. Livius
Fürst, Virchow's Archiv, June, 1884.

The symptoms of cerebral disturbance in chronic hydrocephalus are

much less striking than one would expect, doubtless because the
increase of pressure upon the brain is so gradual. Actual paralysis,
especially of the limbs, is rare, but convulsions are not infrequent, as
is the spasmodic constriction of the glottis known as laryngismus
stridulus or spasmodic croup. A general state of uneasiness and
restlessness is common. Vision is often impaired and sometimes
wholly lost. Strabismus is frequently present, or there may be an
involuntary rolling movement of the eyeballs. The pupils are often
dilated and insensible to light. In consequence of the increased
weight of the head, the child is unable to support it, and in most
cases is compelled to keep the bed. Vomiting is common. The
digestive functions are disturbed. Constipation is an almost constant
symptom, and the sphincters are relaxed in the advanced stages of
the disease. Although in some cases, as already stated, the child
may grow fat, the reverse of this is the rule; there is usually
progressive emaciation, especially of the lower extremities.

The duration of the disease varies much in different cases. The

earlier the characteristic symptoms manifest themselves the more
rapid is its course. Most children born hydrocephalic survive but a
few days or weeks. In cases which are more slow in their
development the patient may live some years, and in rare instances
attain adult life. But his feeble vitality usually makes him an easy
prey to the ordinary complaints of childhood, and a large proportion
of cases succumb to inflammation of the lungs or of other organs, to
diarrhœa, whooping cough, or the eruptive diseases. Most of those
who escape these intercurrent maladies perish from defective
nutrition, the result of malassimilation of food, or else are cut off by
acute cerebral inflammation, with convulsions, etc.

PATHOLOGICAL ANATOMY.—It is rarely that a large amount of serum is

found in the cavity of the arachnoid unless a free communication has
been established between it and the ventricles by the destruction of
cerebral tissue. In the pia the quantity may be more abundant than
normal, filling the subarachnoid spaces, separating the convolutions
from each other, and occasionally forming little sac-like elevations on
the surface of the membrane; but it should be borne in mind that a
certain amount of serous infiltration of the tissue of the pia is by no
means rare in cases of death from various diseases, owing to the
obstruction to the circulation during the last hours of life, and should
not be considered pathological unless it exceed the usual limits. The
amount of effusion into the ventricles varies between very wide
limits, from some ounces to two or three pints. It may be transparent,
or turbid from particles of cerebral tissue or epithelial or pus-cells,
and is occasionally slightly tinged with blood. Its specific gravity is
nearly identical with that of water, and it contains a trace of albumen.
The effusion usually occupies the two lateral and the middle
ventricles. Less frequently the dropsy is unilateral, in consequence,
apparently, of an obliteration of the foramen of Monro. The tissues
composing the walls of the ventricles are compressed and hardened.
The ependyma of the walls and of the plexus is thickened and
roughened by the formation of minute elevations, which the
microscope shows to be composed of proliferated and sclerosed
connective tissue. The brain in cases of large effusion is reduced to
a membranous sac, flattened, with hardly any trace of its original
structure at first sight apparent. In the case of James Cardinal,
before alluded to, Bright says, “The brain lay at its base [of the skull]
with its hemispheres opened outward like the leaves of a book.”
Closer inspection shows that all the parts are present, although
atrophied by pressure. The convolutions are flattened and the brain-
substance is pale and softened. The cranial nerves are often
softened and flattened.

In the dropsy of the head in adults which is the result of mechanical

pressure or of cachexia the appearances are widely different. The
effusion may occupy the cavity of the arachnoid, and even the space
between the dura and the skull, as well as the ventricles. The
amount of fluid is much less than in the chronic hydrocephalus of
children. The ventricular walls present no signs of inflammatory
changes.

DIAGNOSIS.—Chronic hydrocephalus is usually recognized without

difficulty. The chief points of diagnostic importance are the
progressive enlargement of the head, the separation of the cranial
bones, with their peculiar change of position, as already described,
and the evident signs of arrested intellectual development. If the
head be but little enlarged, the case might be mistaken for that of
chronic hypertrophy of the brain, but this is a very rare disease, and
is not accompanied with defective mental development.

PROGNOSIS.—The elements of prognosis include the size of the head

at birth, its rate of enlargement, the general condition of the child,
both physically and intellectually, his hereditary antecedents, and the
hygienic influences to which he may be subjected. A large proportion
of children born hydrocephalic live but a short time; a few survive
one or more years. The number of those who reach adult life is
extremely small. The favorable indications are a tardy appearance of
the dropsy and its slow progress, without marked evidence of
defective mental and bodily development.

TREATMENT.—The treatment of chronic hydrocephalus is general and

local, the first being the most important, although in many cases it is
difficult to enforce it, from lack of intelligence and of means on the
part of those in charge of the patient. Proper ventilation, good
drainage, and cleanliness are essential. The child should be bathed
daily, and should be protected against changes in temperature by
suitable clothing. If his strength allow, he should be taken into the
open air daily in fine weather. A wet-nurse should be provided for
infants whose mothers are unable to suckle them. Older patients
should take milk, cream, animal broths, farinaceous substances,
etc., with wine or brandy. Tonics, especially cod-liver oil,
hypophosphite of lime, and some preparation of iron or of the iodide
of iron, are important, the choice being determined by the effect
apparently produced. The internal and external employment of
mercurial preparations, once in vogue, is now almost entirely
abandoned by the best authorities. The evacuation of the fluid by
puncture, followed by compression of the head by bandaging, has
been occasionally resorted to, and in a few instances with success,
but the cases in which it is indicated are rare. Thomas Young
Thompson6 reports a case in which puncture was followed by
recovery. The child, fourteen days old, fell, apparently without ill
effects, but three weeks afterward a protuberance appeared on the
crown of the head which continued to enlarge, and the signs of
chronic hydrocephalus were unmistakable. In three months the
circumference over the parietal eminences measured 20 inches, and
a year afterward 24½ inches. In spite of energetic internal and
external treatment the enlargement continued to progress, until the
head was punctured, and about three hundred grammes of a clear,
transparent fluid, free from albumen, were evacuated. Five weeks
later a second puncture was made, and sixty grammes of a milky
fluid withdrawn. The child recovered, and two years later was in
good health, the head not being disproportioned to the rest of the
body. West considers the cases in which the effusion is apparently
external—that is, confined to the arachnoid cavity, rather than
ventricular, and in which there are no indications of active cerebral
disease—to be the most favorable for the operation. The proper
situation for the puncture is the coronal suture, about an inch or an
inch and a half from the anterior fontanel. A few ounces of fluid only
should be withdrawn at a time, and compression should be carefully
applied both during the escape of the fluid and afterward.
6 Med.-Chir. Transactions, vol. xlvii., 1864.
 CONGESTION, INFLAMMATION, AND
HEMORRHAGE OF THE MEMBRANES OF THE
SPINAL CORD.

BY FRANCIS MINOT, M.D.

Congestion of the Spinal Membranes.

The blood-vessels of the spinal membranes communicate freely with

the general circulation, and there is less opportunity for their
obstruction than in the case of the meninges of the brain.
Hyperæmia of the dura and pia mater is therefore seldom met with,
except in connection with disease of the cord; and, indeed, but little
is known on the subject, which is only alluded to as possible by
authorities of the present day, although the affection was formerly
supposed to be a common one, giving rise to various symptoms,
such as numbness and formication of the extremities, muscular
weakness, and even paraplegia—symptoms which are now known
to be caused by structural diseases of the cord only. As Erb1
remarks, “It is hardly possible that any considerable hyperæmia of
the meninges should exist without a similar condition existing in the
cord also, as the vascular supply of both is the same.”
 1 “Krankheiten des Rückenmarks,” von Wilhelm Erb, in Ziemssen's Handbuch,
Leipzig, 1876; Am. trans., vol. xiii. p. 99.

ETIOLOGY.—Hyperæmia of the spinal membranes is found after death

from convulsions, especially in cases of tetanus, hydrophobia,
eclampsia, strangulation, poisoning from narcotics, etc., in which the
effect is evidently due to asphyxia. An interesting case of extensive
hyperæmia of the spinal membranes, as well as of those of the
brain, complicating mania, is reported by M. R. G. Fronmüller.2 A girl
of eighteen years, previously well, being accused of theft, fell into a
state of melancholia, passing into mania, with frequent convulsions,
screaming, etc. There was no spinal tenderness. The urine
contained no albumen. The temperature was never elevated. No
opisthotonos. The sphincters became relaxed, and she died at the
end of about three weeks. The dura was found to be normal, but the
pia mater of the brain, cerebellum, medulla oblongata, and cord was
strongly injected. The brain and cord were normal; no ventricular
effusion. Here the meningeal hyperæmia was doubtless caused by
asphyxia resulting from the convulsions.
2 See Schmidt's Jahrbücher, 1883, No. 7.

Congestion of the spinal membranes has been attributed to sudden

suppression of the menstrual flow or of hemorrhoidal bleeding, and
to portal obstruction, but the evidence of this is very meagre.
Exposure to cold and wet, as from sleeping on the damp ground, is
an alleged and plausible cause.

The SYMPTOMS attributed to hyperæmia of the spinal membranes are

pain in the back extending to the legs, with numbness and tingling of
the toes, sensation of weight in the limbs, muscular weakness,
appearing suddenly without fever and usually of transient duration.
There is no evidence that it gives rise to paralysis. Considering that
temporary congestion of the membranes must occasionally happen
from convulsions, as in epilepsy, etc., it is remarkable that no
symptoms attributable to it have been observed under these
circumstances.3
 3 See Epilepsy and other Chronic Convulsive Diseases, etc., by W. R. Gowers, M.D.,
London, 1881, p. 106.

MORBID ANATOMY.—We must be careful not to mistake post-mortem

staining of the tissues from imbibition of the coloring matter of the
blood—the result of decomposition aided by the position of the body
—for true congestion. The latter is recognized by fine vascular
arborization covering the surface of the dura or pia, often
accompanied with small punctate hemorrhages. More extensive
extravasations in the connective tissue, surrounding and between
the membranes, are sometimes found. The spinal fluid is usually
increased in amount, and often tinged with red. On account of the
free vascular connection between the membranes and the cord the
latter almost always partakes of the congestion.

DIAGNOSIS.—From what has been said it follows that simple

hyperæmia of the spinal membranes can hardly be distinguished
from that of the cord. (See the article on DISEASES OF THE SUBSTANCE
OF THE BRAIN AND SPINAL CORD.) When the symptoms are
unaccompanied by fever, are of very moderate severity, and of short
duration, we may perhaps infer that the lesion is confined to the
membranes.

The TREATMENT is the same as that for congestion of the spinal cord.

Acute Inflammation of the Spinal Dura Mater.

SYNONYM.—Acute spinal pachymeningitis.

Acute inflammation of the spinal dura mater is chiefly confined to the

outer surface of the membrane (peripachymeningitis), and is almost
always consecutive to either injury or disease of the vertebræ
(fracture, dislocation, caries), to wounds penetrating the spinal
cavity, or to suppurative disease in neighboring organs or tissues,
which makes its way into the peridural space through the
intervertebral openings. The symptoms are complex—in part caused
by the original disease, and in part by the pressure of the products of
inflammation exercised upon the nerve-roots, and even upon the
cord itself. Pain in the back, corresponding to the seat of the
disease, is rarely absent, and all movements of the trunk are
extremely painful. When the exudation is sufficient to compress the
nerve-roots, the pain will extend to the trunk and the limbs, and other
signs of irritation, such as a feeling of constriction by a tight girdle,
and tingling, numbness, and cutaneous hyperæsthesia in the limbs,
will be observed, varying in situation according to the seat of the
lesion. In some cases the compression of the cord may be sufficient
to cause paraplegia. General symptoms will vary according to the
complications of the case. Severe injury or extensive disease of the
vertebræ will be accompanied with high fever; but if the external
inflammation be moderate and the meningeal complication be limited
in extent, the fever may be subacute.

MORBID ANATOMY.—The connective tissue between the dura and the

bone is the seat of inflammatory exudation, usually purulent, of
greater or less extent, and more abundant in the posterior than the
anterior part of the spinal cavity, owing to the position of the patient.
A more or less abundant exudation, either of pus or of dry caseous
matter, is found upon the outer surface of the dura or infiltrating the
connective tissue between it and the bony walls. The dura is
thickened, and sometimes the exudation is seen upon its inner walls,
but the pia is seldom involved in the inflammation. The cord may be
compressed or flattened when the amount of exudation is large, and
may in consequence show signs of inflammation in its vicinity. The
spinal nerves likewise are sometimes compressed, atrophied,
softened, and inflamed. The disease rarely occupies the cervical
region, on account of the close union of the dura with the bones of
that part; hence there is an absence of pain in the neck and of
retraction of the head.

DIAGNOSIS.—The diagnosis is founded on the presence of general

symptoms of spinal disease—pain in the back, but not extending to
the neck, increased by movements of the trunk; cutaneous
hyperæsthesia, tingling, or numbness in various parts of the surface
of the body; paresis or paralysis of the lower extremities in severe
cases; along with a history of vertebral disease or injury or of
suppurative disease in the neighborhood of the spine. The history of
the case will generally be sufficient to exclude myelitis, tetanus, or
muscular pain (rheumatism, lumbago). From acute leptomeningitis
the diagnosis must also be made by the history, but it should be
borne in mind that the pia may be involved at the same time with the
dura.

PROGNOSIS.—In complicated cases the prognosis is grave if the

spinal symptoms are well marked and severe, especially when there
is evidence of much pressure on the cord (paraplegia). If the signs of
spinal irritation were moderate, the danger would depend upon the
nature and extent of the external lesion.

TREATMENT.—This would be addressed mainly to the primitive

disease. For the spinal symptoms the treatment would not differ
materially from that of inflammation of the spinal pia mater.

Chronic Spinal Pachymeningitis.

This affection generally coexists with chronic inflammation of the pia.

Like the acute inflammation of the dura, it is seen in connection with
disease or injury of the vertebræ, and it may also arise from tumors
of the membrane (chiefly syphilitic) and from myelitis. It is frequent
among the chronic insane, and in them is sometimes associated with
hemorrhagic effusions analogous to the hæmatoma of the cerebral
dura mater. Chronic inflammation of the spinal dura is of unfrequent
occurrence, and but little is known of its history and pathology. In a
case reported by Wilks4 the membrane was thickened to nearly its
whole extent, and in the cervical region presented numerous bony
plates. The pia was also thickened at this part and adhered closely
to the dura. The symptoms, which seemed chiefly due to disease of
the cord from compression, were retraction of the lower limbs and
violent jerking from excessive reflex action.
4 Transactions of the Pathological Society of London, vol. vii., 1856.

A special form of the disease, occupying chiefly the cervical region,

was first described by Charcot.5 The membrane is thickened by a
deposit of successive layers of fibrin, compressing the cord, which is
flattened from before backward and inflamed. The nerve-roots are
also more or less compressed. The course of the disease may be
divided into two stages: First, that of irritation of the spinal nerves,
with pain in the back part of the neck, extending to the head and
along the upper limbs. The pain is permanent, but liable to
exacerbations, and is accompanied with stiffness of the neck and a
feeling of numbness and tingling, with muscular weakness of the
arms. Sometimes the skin of the arms is the seat of trophic changes,
as shown by the presence of bullæ or pemphigus. The second
period is that of extension of the disease to the cord. The pain
ceases, and is followed by paralysis or muscular atrophy, especially
in the domain of the ulnar and median nerves, resulting in extension
of the hand on the forearm, with flexion of the fingers toward the
palm, giving rise to a claw-like appearance (main en griffe). In some
cases an upward extension of the disease implicates the root of the
radial nerve, and the hand then assumes a prone position from
paralysis of the extensor muscles. The lower portion of the cord may
also become involved, with similar results in the lower extremities.
Although the disease is generally progressive, it is not always so,
and Charcot cites one case in which great improvement took place in
the course of some years, though not apparently in consequence of
any special treatment.
5 Leçons sur les Mal. du Syst. nerv., par J. M. Charcot, Paris, 1875, vol. ii. p. 246.
See, also, Maladies du Syst. nerv., par A. Vulpian, Paris, 1879, p. 127; and Clinique
méd. de l'Hôpital de la Charité, by the same.