630 • ENDOCRINOLOGY

Hands

Palmar erythemaTremorAcromegalyCarpal tunnel syndrome

Skin

Hair distributionDry/greasyPigmentation/pallorBruisingVitiligoStriaeThickness

Pulse

Atrial fibrillationSinus tachycardiaBradycardia

Breasts

GalactorrhoeaGynaecomastia

Neck

Voice Hoarse, e.g. hypothyroid VirilisedThyroid gland (see opposite) Goitre Nodules

8

7

7

8

9

10

11

12

6

2

3

4

5

Observation• Most examination in endocrinology is by observation• Astute observation can often yield ‘spot’ diagnosis of endocrine disorders• The emphasis of examination varies depending on which gland or hormone is thought to be involved

Body fat

Central obesity in Cushing’ssyndrome and growth hormonedeficiency

9

Height and weight

Bones

Fragility fractures (e.g. ofvertebrae, neck of femur ordistal radius)

10

Genitalia

VirilisationPubertal developmentTesticular volume

11

Legs

Proximal myopathyMyxoedema

12

Blood pressure

Hypertension in Cushing’sand Conn’s syndromes,phaeochromocytomaHypotension in adrenalinsufficiency

Eyes Graves’ disease (see opposite) Diplopia Visual field defect (see opposite)Hair Alopecia Frontal balding

Facial features Hypothyroid Hirsutism Acromegaly Cushing’s

1

Prognathism inacromegaly

Acromegalic hands. Note softtissue enlargement causing‘spade-like’ changes

Pigmentation of creasesdue to high ACTH levelsin Addison’s disease

Vitiligo in organ-specificautoimmune disease

Multinodulargoitre

Pretibial myxoedemain Graves' disease

Head

Mental state Lethargy Depression Delirium Libido

1

2

3

4

5 6

Clinical examination in endocrine disease

Endocrine disease causes cl inical

syndromes with symptoms and signs

involving many organ systems. The

emphasis of the clinical examination

depends on the gland or hormone that

is thought to be abnormal.

Diabetes mellitus (described in detail in

Ch. 20) and thyroid disease are the most

common endocrine disorders.

Clinical examination in endocrine disease • 631

18

6 Examination of the visual fields by confrontation

• Sit opposite patient• You and patient cover oppositeeyes

• Bring red pin (or wiggling finger)slowly into view from extreme ofyour vision, as shown

• Ask patient to say ‘now’ when itcomes into view

• Continue to move pin into centreof vision and ask patient to tellyou if it disappears

• Repeat in each of four quadrants• Repeat in other eye

A bitemporal hemianopia is theclassical finding in pituitarymacroadenomas (p. 683)

6 Examination in Graves’ ophthalmopathy

• Inspect from front and side Periorbital oedema (Fig. 18.8) Conjunctival inflammation (chemosis) Corneal ulceration Proptosis (exophthalmos)* Lid retraction*

• Range of eye movements Lid lag on descending gaze* Diplopia on lateral gaze

• Pupillary reflexes Afferent defect (pupils constrict further on swinging light to unaffected eye, Box 25.22)

• Vision Visual acuity impaired Loss of colour vision Visual field defects

• Ophthalmoscopy Optic disc pallor Papilloedema

*Note position of eyelids relative to iris.

Normal

Proptosis

Right proptosis and afferent pupillary defect

Lidretraction

Normal

Normaldescent

Lid lagdescent

7 Examination of the thyroid gland

Diffuse firm goitre Hashimoto’s thyroiditis (p. 646)

Diffuse tender goitre Subacute thyroiditis (p. 646)

Abnormal findings

Diffuse soft goitre with bruit Graves’ disease (p. 643)

Multinodular goitre (p. 648) ± Retrosternal extension, tracheal compression

Solitary nodule (p. 642) Adenoma, cyst or carcinoma

Cervical lymphadenopathy Suggests carcinoma

• Inspect from front to side

• Palpate from behind Thyroid moves on swallowing Check if lower margin is palpable Cervical lymph nodes Tracheal deviation

• Auscultate for bruit Ask patient to hold breath If present, check for radiating murmur

• Percuss for retrosternal thyroid

• Consider systemic signs of thyroid dysfunction (Box 18.7) incl. tremor, palmar erythema, warm peripheries, tachycardia, lid lag

• Consider signs of Graves’ disease incl. ophthalmopathy, pretibial myxoedema

• Check for Pemberton’s sign, i.e. facial engorgement when arms raised above head

720 • DIABETES MELLITUS

Clinical examination of the patient with diabetes

Insets ( Acanthosis nigricans) From Lim E (ed.). Medicine and surgery: an integrated textbook. Edinburgh: Elsevier Ltd; 2007. ( Exudative maculopathy)

Courtesy of Dr A.W. Patrick and Dr I.W. Campbell.

Blood pressure

Skin

BullaePigmentationGranuloma annulareVitiligo

Axillae

Neck

Carotid pulseBruitsThyroid enlargement

Eyes (see opposite)

Visual acuityCataract/lens opacityFundoscopy

Insulin injection sites

(see opposite)

Hands

(see opposite)

Feet (see opposite)

InspectionPeripheral pulsesSensation

Abdomen

Hepatomegaly(fatty infiltration of liver)

Legs

Muscle-wastingSensory abnormalityHair lossTendon reflexes

Exudative maculopathy

Necrobiosis lipoidica

Charcot neuroarthropathy

Neuropathic foot ulcer

Head

XanthelasmaCranial nerve palsy/eyemovements/ptosis

Observation• Weight loss in insulin deficiency• Obesity in type 2 diabetes• Mucosal candidiasis• Dehydration– dry mouth, ↓tissue turgor• Air hunger– Kussmaul breathing in ketoacidosis

2

3

1

11

10

9

4

5

6

7

1

2

3

5

7 8

9

10

11

6

4

8

Acanthosis nigricans

in insulin resistance

‘Prayer sign’

Clinical examination of the patient with diabetes • 721

20

Diabetes can affect every system in the

body. In routine clinical practice, exam-

ination of the patient with diabetes is

focused on hands, blood pressure, axillae,

neck, eyes, insulin injection sites and feet.

1 Examination of the hands

Several abnormalities are more common in

diabetes:

• Limited joint mobility (‘cheiroarthropathy’)

causes painless stiffness. The inability to

extend (to 180°) the metacarpophalangeal

or interphalangeal joints of at least one

finger bilaterally can be demonstrated in

the ‘prayer sign’

• Dupuytren’s contracture (p. 1059) causes

nodules or thickening of the skin and

knuckle pads

• Carpal tunnel syndrome (p. 1139)

presents with wrist pain radiating into

the hand

• Trigger finger (flexor tenosynovitis) may

be present

• Muscle-wasting/sensory changes may be

present in peripheral sensorimotor

neuropathy, although this is more

common in the lower limbs

Background retinopathy. Courtesy of Dr

A.W. Patrick and Dr I.W. Campbell.

Proliferative retinopathy. Courtesy of Dr

A.W. Patrick and Dr I.W. Campbell.

7 Examination of the eyes

Visual acuity

• Check distance vision using Snellen chart

at 6 m

• Check near vision using standard reading

chart

• Note that visual acuity can alter reversibly

with acute hyperglycaemia due to osmotic

changes affecting the lens. Most patients

with retinopathy do not have altered

visual acuity, except after a vitreous

haemorrhage or in some cases of

maculopathy

Lens opacification

• Look for the red reflex using the

ophthalmoscope held 30 cm from

the eye

Fundal examination

• Either use a three-field retinal camera or

dilate pupils with a mydriatic (e.g.

tropicamide) and examine with an

ophthalmoscope in a darkened room

• Note features of diabetic retinopathy

(p. 1174), including photocoagulation

scars from previous laser treatment

8 Insulin injection sites

Main areas used

• Anterior abdominal wall

• Upper thighs/buttocks

• Upper outer arms

Inspection

• Bruising

• Subcutaneous fat deposition

(lipohypertrophy)

• Subcutaneous fat loss (lipoatrophy;

associated with injection of unpurified

animal insulins – now rare)

• Erythema, infection (rare)

Lipohypertrophy of the upper arm.

11 Examination of the feet

Inspection

• Look for evidence of callus formation on

weight-bearing areas, clawing of the toes

(in neuropathy), loss of the plantar arch,

discoloration of the skin (ischaemia),

localised infection and ulcers

• Deformity may be present, especially in

Charcot neuroarthropathy

• Fungal infection may affect skin between

toes, and nails

Circulation

• Peripheral pulses, skin temperature and

capillary refill may be abnormal

Sensation

• This is abnormal in stocking distribution in

typical peripheral sensorimotor neuropathy

• Testing light touch with monofilaments is

sufficient for risk assessment; test other

sensation modalities (vibration, pain,

proprioception) only when neuropathy is

being evaluated

Reflexes

• Ankle reflexes are lost in typical

sensorimotor neuropathy

• Test plantar and ankle reflexes

Monofilaments. The monofilament is

applied gently until slightly deformed at five

points on each foot. Callus should be

avoided as sensation is reduced. If the

patient feels fewer than 8 out of 10

touches, the risk of foot ulceration is

increased 5–10-fold.

346 • CLINICAL BIOCHEMISTRY AND METABOLIC MEDICINE

Clinical examination in biochemical and metabolic disorders

Many biochemical and metabolic disorders are clinically silent or present with non-specific manifestations, and are first detected by

laboratory testing. Several abnormalities can be picked up by history and physical examination, however, as summarised below.

Insets: (ankle oedema) From Huang H-W, Wong L-S, Lee C-H. Sarcoidosis with bilateral leg lymphedema as the initial presentation: a review of the

literature. Dermatologica Sinica 2016; 34:29–32; (raised jugular venous pressure) Newby D, Grubb N. Cardiology: an illustrated colour text. Edinburgh:

Churchill Livingstone, Elsevier Ltd; 2005; (cherry-red spots) Vieira de Rezende Pinto WB, Sgobbi de Souza PV, Pedroso JL, et al. Variable phenotype and

severity of sialidosis expressed in two siblings presenting with ataxia and macular cherry-red spots. J Clin Neurosci 2013; 20:1327–1328; (photosensitive

rash) Ferri FF. Ferri’s Color atlas and text of clinical medicine. Philadelphia: Saunders, Elsevier Inc.; 2009; courtesy of the Institute of Dermatology, London.

Hyperlipidaemia

Xanthelasma

Corneal arcus

Gangliosidosis

Cherry-red spot fundus

Porphyria

Photosensitive rash

Hyperlipidaemia

Tendon xanthoma

Eruptive xanthoma

Observation• General appearance• Skin turgor• Oedema• Rash• Eyes

Hypervolaemia

Raised jugular venouspressure

Ankle oedema

Hypovolaemia

Low blood pressure

Rapid pulse

Acute hypernatraemia

Extra heart soundsDizzinessDeliriumWeakness

Acute hyponatraemia

Cerebral oedemaVomitingSomnolenceSeizuresComa

Glycogen storage disease

Hepatomegaly

Abdominal pain

Extra heart sounds

Atheroma

Lung crepitations

B

C

N

O

P

A

K

L

I

M

J

D

E

F

G

H

H

G

K

N

O

P

D

C

B

A

J J

L

M

F

I

E

Clinical examination in biochemical and metabolic disorders • 347

14

Assessment of volume status and electrolyte disturbances

Check blood pressure, pulse and jugular venous pressure Check for dry mouth

Check for sacral and ankle oedema Examine chest for pleuraleffusion

Examine abdomen forhepatomegaly and ascites

Check bloods Review results Check ECG Hypokalaemia Hyperkalaemia

Check skin turgor

Check for signs of hyperlipidaemia

Check skin and tendons for xanthomas Check eyes for arcus and xanthelasma

PeakedT wave

U wave

STdepression

692 • NUTRITIONAL FACTORS IN DISEASE

Insets (Scaphoid abdomen) From Chandra A, Quinones-Baldrich WJ. Chronic mesenteric ischemia: How to select patients for invasive treatment. Sem Vasc

Surg 2010; 23:21–28; (Koilonychia) Habif TP. Clinical Dermatology, 6th edn. Philadelphia: Saunders, Elsevier Inc.; 2016; (Gingivitis) Newman MG, Takei H,

Klokkevold PR, et al. Carranza’s Clinical Periodontology, 12th edn. Philadelphia: Saunders, Elsevier Inc.; 2015; (Corkscrew hairs) Bolognia JL, Jorizzo JL,

Schaffer JV, et al. Dermatology, 3rd edn. Philadelphia: Saunders, Elsevier Inc.; 2012.

Eyes

Sunken eyesPallorJaundiceBitot spots (↓vitamin A;see Fig. 19.12)

Hands

Muscle wasting (dorsal interossei,thenar eminences)Finger clubbingLeukonychia (low albumin)Koilonychia (iron deficiency)

Simple anthropometrics(see right)

Body mass indexTriceps skin fold thicknessWaist circumference

Legs

Pitting oedemaUlcers

Affect

FatigueDepressionDementia

Mouth

PallorAngular stomatitis (↓B12, folate,iron)Glossitis (↓B12, folate, iron)Gingivitis, bleeding gums(↓vitamin C; see Fig. 19.14)Poorly fitting dentures

Corkscrew hairs

Gingivitis

Koilonychia

Scaphoid abdomen

Clinical effects of short bowelsyndrome after multipleresection in Crohn’s disease

5

4

6

7

8

3

2

1

43

2

5

6

8

Skin

Dry, flaky skin or dermatitis (seeFig. 19.13)Hair lossSpecific abnormalities: Petechiae, corkscrew hairs (↓vitamin C) Dermatitis of pellegra (↓niacin)

7

Observation

Signs of weight loss: Prominent ribs Muscle wasting ↓Skin turgor

1

Clinical examination in nutritional disorders

Clinical assessment and investigation of nutritional status • 693

19

Clinical assessment and investigation of nutritional status

Important elements of the diet history

Ask about weight

• Current weight

• Weight 2 weeks, 1 month and 6 months

ago

• Assessment of degree of change

Ask about current food intake

• Quantity of food and if any change

• Quality of food taken

• Whether normal food is being eaten

• Avoidance of specific food types (e.g.

solids)

• Any nutritional supplements

• Reliance on supplements/tube feeding

• Any change in appetite or interest in

food

• Any taste disturbance

Ask about symptoms that interfere with eating

• Oral ulcers or oral pain

• Difficulties swallowing

• Nausea/vomiting

• Early satiety

• Alteration in bowel habit

• Abdominal (or other) pain

Ask about activity levels/performance status

• Normal activity

• Slightly reduced activity

• Inactive < 50% of the time

• Inactive most of the time

Under-nutrition can go unnoticed in

patients with multiple comorbidities. It is

vital to be aware of under-nutrition as a

potential reason for any acute medical

presentation or as a modifier of it. Early

nutritional assessment is crucial and a

dietary history provides useful information

(especially when taken by a dietitian). Points

to note include past medical and surgical

history (e.g. abdominal or intestinal surgery),

a drug history and a specific diet history.

Evidence of recent weight loss and muscle

wasting should be sought. Simple, validated

tools are available to screen patients for

nutritional problems. Body composition

reflects energy balance and is assessed

by clinical anthropomorphic measurements.

More sophisticated techniques may be used

to assess body composition or functional

capacity if required.

2 Body mass index (BMI)

BMIwt kg

ht m=

( )

( )2

Example: an adult of 70 kg with a height of

1.75 m has a BMI of 70/1.752 = 22.9 kg/m2

• BMI is a useful way of identifying under- or

over-nutrition but cannot discriminate

between lean body or muscle mass and fat

mass

• Fat mass is also subject to ethnic variation;

for the same BMI, Asians tend to have

more body fat than Europeans

• If height cannot be determined (e.g. in older

people or those unable to stand),

measurement of the femoral length or ‘knee

height’ is a good surrogate

Measurement of knee height.

2 Measures of body composition and nutritional status

Body composition

• Anthropometry (see below)

• Bioelectrical impedance

• Dual X-ray absorptiometry (DXA)

Muscle function and global

nutritional status

• Hand grip strength (dynamometer test)

– poor grip associated with increased

mortality

Obesity and fat distribution (android

vs gynoid)

• Waist:hip ratio (circumferences measured

midway between superior iliac crest and

lower border of rib cage, and at greater

trochanters, respectively)

Body fat content and muscle mass

• Triceps skinfold thickness (when combined

with mid-/upper arm circumference

estimates muscle mass)

Triceps skinfold thickness. Lean patients

6–12 mm; obese patients 40–50 mm.

Screening hospitalised patients for risk of malnutrition. Acute illnesses include decompensated liver disease, cancer cachexia or being kept ‘nil by

mouth’. Adapted from the British Association of Parenteral and Enteral Nutrition Malnutrition Universal Screening Tool (www.bapen.org.uk).

Weight loss score

Unplanned loss in 6 months

< 5%5 – 10%> 10%

= 0= 1= 2

BMI score

> 2018.5 – 20

< 18.5

= 0= 1= 2

Acute disease score

Acute illness with nonutritional intakefor 5 days = 2

Total = 1 – Medium riskTotal = 0 – Low risk Total ≥ 2 – High risk

Total score

• Routine clinical care• Repeat screen weekly

• Document dietary intake for 3 days• Repeat screen weekly

• Refer to dietitian/nutrition support team• Review plan weekly