General Physical Examination: performed with situation awareness.

Medical students will also find this useful.

What is the purpose of a GPE (general physical examination)? You are looking for clues or any evidence of a disease. You may be able to diagnose a disease or the clue may point to a group of diseases and then you will have to look for other signs which occur in this disease. The clue is a pointer which will guide the rest of the GPE i.e. it will determine which sign or signs you need to look for next. The more knowledge of diseases and their differential diagnosis you have the better GPE you can do. If you find enlarged lymph nodes in the neck (normal lymph nodes are not palpable: LN less than 1/2 a cm are probably insignificant) you need to check LN in the axilla and groin; look for anemia and weight loss; look for an enlarged spleen and liver; examine the skin for petechial bleeds. You will then do the rest of the GPE and can ignore clubbing which you need only do if you suspect a disease in which clubbing is found like bronchectasis or cyanotic heart disease. The sequence of your examination depends on what you find first. Whenever you read up a disease ask yourself what am I likely to find in the GPE and other clinical examination. Always perform the clinical examination from knowlegde.It helps if you can recognise patterns of signs which occur together. Pattern recognition is an important part of your training both in the history and the physical examination. It is very important that you are not only able to use the correct clinical methods to elicit information but that you understand what you are doing and can explain the basis of the sign physiologically and understand the pathology behind it. If you are ignorant of what a sign means or signifies then you are not going to do well in an examination and as a physician your patient is not going to benefit from your so-called expertise.

Why have these abnormalities occurred? What else should one look for? Start your GPE with these questions in mind.

What abnormalities will the GPE help us to find? Look for the most commonly found ones first and then look for the rare ones if it is applicable. For example don’t start by looking for clubbing which you are likely to find in one out of two hundred patients and if you miss it you are not likely to cause harm. If you forget to check the pulse or the BP you can really injure the patient. The common abnormalities are:

  • Distress, posture, facies. Observe the patient first. 
    • Is there pain and what is likely to aggravate it. Provide pain relief with appropriate medication. Ensure you examine the patient in the posture which is most comfortable for them. This is specially true for any form of arthritis.
    • Breathlessness. Breathlessness or shortness of breath.( PLease do not write SOB because that is short for “son of a bitch”). Have the patient sitting up or in a head up reclining position. Do not insist that the patient lie flat for an abdominal or chest examination if they are breathless. If you do this the patient may be in danger of dying and you will definitely fail the exam.
    • Wheezing, pursing of the lips and cough. Note whether the patient is expectorating. Offer him a spittoon and look at the expectorant. This direct observation will save you from asking too many questions.
    • Pruritus. Itching can be a prominent feature of many diseases including chronic renal failure. Note if the patient is scratching himself, look for scratch marks and excoriation.
    • Listlessness, depression and a disinclination to give you the information you require. This is often a “cry for help”. The patient feels nothing is going to make him better and is resigned to his fate. Reassure him, try to cheer him up and give him some positive input to get him to cooperate. Talk to a caregiver and try to get them to reassure the patient.
    • Note the posture, gait and the angle of the limbs and joints.
    • Agitation, hyperactivity, over talkativeness. This may be part of the disease or caused by the anxiety of talking to a doctor. Calm the patient down first and use pharmacological help if the disease permits. It may be caused by hyperthyroidism or may be the effect of a drug.
    • The patient’s facial configuration or facies: flushed cheeks, ruddy face, moon-faced, emaciated cheeks, prominent eyes, pattern of baldness if present, any eruptions on the face or scalp, droopy eyelid, immobility of half the face, or immobility or partial immobility of an eye, congenital abnormality. You do not have to sing out a list of all these, just look for them and then say the patient has no facial abnormality or special facies.
    • Tremor or abnormal movement. Note whether this occurs at rest or during movement, whether the range is small and rapid (fine tremor) or slower and larger range (coarse) and if there is a twisting or torsion movement.
    • Mention any other abnormality such as a bleeding tendency or rash or bruising etc.
    • Changes in colour. The patient may be obviously jaundiced or cyanosed. Mention this first. A waxy darkening of the skin is known as a sallow complexion. This is often noticed in chronic kidney disease specially in inadequately dialysed patients.
  • Fever is common, so check the temperature in the axilla (remember  you do not want to spread the hepatitis viruses). Fever can be caused by an infection, an inflammatory condition, infarcts, malignancies or may even be drug induced. You do not need an antibiotic for every fever. Plan what investigations you will do for fever. It may be worthwhile not to prescribe an antibiotic but you can use paracetamol to keep the patient comfortable. With the array of tests available to us it is usually unnecessary to “observe a pattern of fever” . Remember the pronunciation is  “pat urn not pat ren”.
  • Changes in the  blood pressure. Check the BP.
    • High blood pressure is silent so it needs to be looked for. It becomes more frequent in older patients but can occur at any age even infants , adolescents, pregnant women. It may be an isolated finding or part of a disease like glomerulonephritis,  other renal diseases, eclampsia. A high BP is often found in diabetes and also in heart failure. Looking for evidence of congestive cardiac failure or evidence of kidney diseases is part of situational awareness. If the BP is high examine the fundus occuli where blood vessels can be seen and damage done to them by hypertension can also be seen in them. Exudates and hemorrhages in the retina are also evidence of damage to capillaries caused by a rapid rise in BP. So you can explain whether the damage is in the arteries or capillaries. If the BP is high look for pedal edema, a raised JVP, crackles in the lung bases and an enlarged liver and a fourth heart sound. These signs are  grouped together and   are signs of heart failure. So if the major finding is a high BP and the history also points to CCF then look for these signs in a group. Check every patient’s BP/
    • A low BP should make you look for postural drop i.e. if the standing systolic BP falls by 20 mmHg then the patient needs continuous monitoring so will be better managed in an ICU, with access to a cardiac monitor or a round the clock nurse and an IV life line must be started. A blood transfusion may be needed and the urine output must be monitored so don’t just note the low BP do something about it. This is situational awareness.
  • Changes in the pulse. Tachycardia is a pulse above 110/min and bradycardia a pulse below 60/min. Tachycardia is commonly seen in fever (the pulse rises 10 beats/min for every degree rise in body temperature above 98 degrees Farenheit. A higher rise is called undue tachycardia and is often found in myocarditis or septicemic shock). Tachycardia occurs after exercise, in pregnancy, in heart failure, in anemia, hyperthyroidism, shock and anxiety. in a patient with typhoid fever undue tachycardia should alert you to involvement of the heart myocarditis or an internal bleed or intestinal rupture. In any critically ill patient tachycardia not caused by fever should make you look for aspiration pneumonia, internal hemorrhage or septicemic shock. Remember that in severe septicemia there may be no fever only shock. Remember the tachy arrhythmias. Monitor the BP in these patients. do repeated ECG or use a cardiac monitor,  check the cardiac enzymes, check the Hb repeatedly. Do a portable X-ray chest. See how a simple finding in the GPE will guide your management! Note any irregularity in the pulse and learn to recognise the patterns of irregularity. The most common one you are going to pick up is atrial fibrillation.
  • Anemia: look for weight loss, icterus, evidence of bleeding like piles, petechae, nose bleeds and bleeding on gums, and enlarged LNs. If you find kolionychia then iron deficiency is likely. Take a dietary history (do they manage to eat iron rich red meat, chicken or dal? How often) and a history of bleeding (menstrual bleeding in women and piles in men and women), suspect worms if the patient works barefoot in a rural environment. You can always ask additional questions in the history.
  • Jaundice. Is it accompanied by anemia (hemolytic anemia), signs of chronic liver disease, hard splenomegaly (think of a hemolytic anemia)? Is there an accompanying weight loss and loss of appetite? This is pattern recognition.  Think of obstructive jaundice associated with gallstones, a malignancy of the pancreas, gall bladder, pancreatic duct  (the ampulla of Vater), infiltrative malignancy of the liver specially metastasis.  Cholestatic jaundice can also occur in pregnancy, with drugs,in alcoholism,  in viral hepatitis, AIDS cholestasis, with extravasated blood in the tissues as in massive infarct and advanced liver failure. Look up the rest in your book.
  • Weight. Check the weight and establish a weight baseline. In future you can see if the patient is gaining or losing weight. This is specially important to establish water retention and whether diuretics are helping. A weight loss of 1/2 a kg per day in a patient with ascites or edema indicates that your diuretic therapy is effective. If it is less than that then increase your diuretic dosage, if more than that then reduce your diuretic or you will cause shock and hyponatremia and dehydration. Establish, from a reliable nomogram, whether your patient is overweight or underweight. Work out the BMI. You need the weight to work out the dose of some drugs specially steroids, cancer chemotherapeutic agents, rifampicin etc. In diabetes the dietary advice will depend on the weight: in overweight diabetics you will advise a low-calorie diet with restricted chappatis, rice and sugar while in an underweight diabetic you will advise extra carbohydrates to help gain weight and increase the insulin dosage in order to allow the body to use the carbs. Don’t forget to weigh the patient. You can only skip this if the patient is unable to stand or is unconscious.

Viva question: you are treating a patient with fluid retention caused by heart failure. The patient is unable to stand on a weighing scale. How will you know that your diuretic therapy is effective?

  • Cyanosis. Be very careful while examining a patient with cyanosis. They are obviously not getting enough oxygen to the peripheral tissues and the brain. Cyanosis occurs when there is more than 5gm/dl of deoxygenated hemoglobin in circulation. Hence you can see that a person with 3 gm/Hb will be breathless but not cyanosed. In central cyanosis the extremities are WARM and blue and the tongue is blue too. The tongue gets a rich blood supply from several arteries and it stays in the mouth so it does not get cold. Central cyanosis is caused by inadequate gas exchange in the lungs or admixture of oxygenated and deoxygenated blood as in congenital cyanotic heart disease. You will commonly find this in children and young adolescents and as survival is shortened adults with congenital heart lesions cyanosis are uncommon. In adults PAH (pulmonary artery hypertension) causing reversal of the shunt from left to right initially to right to left as PAH develops occurs in atrial septal defect or VSD. This is called Eisenmenger’s syndrome. The congenital defect known as Ebstein’s anamoly is caused by displacement of the tricuspid valve (inferior and septal cusps) into the right ventricle with resultant early PAH is one form of congenital cyanotic heart disease. These people have often not been cyanotic in childhood. In Ebstein anamoly ASD (secundum) type is a common association with right bundle brand block and preexcitation syndrome on the ECG In adults pulmonary disease such advanced chronic bronchitis and late in all forms of COPD, pulmonary fibrosis, extensive pneumonia, exposure to toxic gases are more likely causes of cyanosis and the cyanosis is usually indicative of  the need for ICU care and oxygen therapy. Cold blue extremities may occur in peripheral vascular disease (think of diabetes or Berger’s disease)or on exposure to cold. Do not diagnose frostbite in Karachi!!!
    • Blue discoloration of the nails may occur in methemoglobinemia and sulph-hemoglobinemia. Read these up.
    • Look for clubbing if the patient has evidence of cyanotic congenital heart disease.

Oral cavity and tongue. You can garner a lot of information from examination of the oral cavity.

  • The tongue shows hydration and can become dry and coated specially in fevers. It can be covered with debris in poor oral hygiene and a black fungus (black hairy tongue) specially in smokers.
    • Thrush. Candida albicans fungus can present as white plaque on the tongue and buccal mucosa which leaves a red painful base if you try to scrape it off.
    • Aphthous ulcers which are red and painful can occur on the tongue, buccal mucosa, palate and gums. They are recurrent, sometimes respond to oral acyclovir and application of a pain relieving gel like Somojel but do not respond to vitamin B Complex.
    • The common cause of a dark line on the edge of the gums is dental plaque but may be a clue to lead poisoning.
    • The colour of the tongue is a clue to disease. Normally the surface is pink and rough from filiform papillae. In iron deficiency the tongue is pale and glossy from loss of the papillae.
    • Cyanosis can be seen on the tongue and on the under-surface a tinge of jaundice may be detected.
    • A smooth, sore, red tongue can be a manifestation of riboflavine deficiency. Pyridoxine deficiency can also cause glossitis, stomatitis and a sore tongue.  Vitamin C deficiency will cause bleeding sore gums with hypertrophy. Most vitamin deficiencies are now in seen in refugee camps or where there has been mass migration of population with consequent starvation, in prisons, after chemotherapy and in patients on parenteral nutrition.
    • A fissured tongue is congenital and usually insignificant and is unlikely to “fall off” as patients fear. A geographical tongue where migratory white patched develop is also insignificant.
    • Examine the tonsillar fossa. In an adult the tonsils should have atrophy. If the tonsil is visible it has the same significance as an enlarged lymph node.
    • The pharyngeal mucosa is normally a pale pink. It may be hyperaemic in acute pharyngitis and may have an ulcer or a patch of grayish membrane as in diphtheria.
    • As the tongue is a muscle or several muscle layers it can atrophy partially (hypoglossal nerve injury) or wholly as in motor neuron disease.
    • Abnormal movement: clonus, athetosis, tremors may be seen in the tongue.
    • Injuries and tumours can be seen in the tongue.
    • Comment on the teeth and the presence of dental caries.
  • Peripheral edema. Swollen feet and swelling around the eyes indicate fluid retention. The patient may have fluid in the pleural or peritoneal cavity as well. Remember fluid is retained ether because the capillary hemodynamics ( the hydrostatic pressure increases or the oncotic pressure rises) accompanied by an increase in capillary permeability as seen in inflammatory edema. In any state where circulation to the kidney is poor the JGA and other sensors react by stimulating the renin-angiotensin-aldosterone secretion and epinephrine as well. So long as the cardiac pump is weak the resultant hypervolemia and hypernatremia do not result in hypertension but restoration if the blood pressure from low to normal. There is retention of IV or oral sodium.  The steady state takes 3-5 days so adjustments are slow, in some edema states the renin levels are not high. This is not well understood. The slow retention of dietary sodium with a vigorous heart pump results in hypertension not edema. There are four major systems which cause fluid retention two occasional ones.
    • The heart. In a failing heart there is inadequate perfusion of the kidneys. THE JGA senses this and secretes angiotensin which also stimulates the aldosterone secretion and indirectly influences ADH secretion. More sodium is picked up by the loop of Henle and distal convoluted tubules.
    • The kidneys. Hypoalbuminemia when the kidney leaks out significant amounts of albumin. The resultant hypo-osmolarity accompanied by leaky capillaries allows fluid to accumulate in the interstitial spaces. In advanced renal failure (ESRD) the glomeruli become sclerosed and the glomerular filtration rate is significantly reduced so no edema occurs.
    • The Liver. Albumin is synthesised in the liver. in cirrhosis and hepatic failure this synthetic function is significantly interfered with so there is low plasma protein oncotic pressure and fluid leaks into the interstitium. As there is portal hypertension the fluid tends to accumulate in the peritoneum first and cause ascites.
    • The pregnant states and premenstrual edema.
    • Other causes:
      • drugs such as minoxidil, calcium channel blockers etc.
      • dependant edema: long haul flights or long drives where the feet are dependant for long periods.

In all forms of fluid retention there is a considerable role of neuroendocrine factors. Aldosterone is secreted in response to low Na in the tubular fluid, ADH is secreted and atrial and brain natriuretic peptide are inhibited.

  • Neck veins. Fulness of the internal jugular vein indicates both fluid overload and right heart failure. the internal jugular vein can be located between the two heads of the sternocleidomastoid at the medial end of the clavical to just behind the angle of the jaw when it maximally full. At the medial end of the clavicle the vessel can accessed for puncture in order to place a CVP (central venous pressure) line for measuring jugular venous pressure and indirectly the right atrial pressure. Measuring the CVP is a useful way to ensure that you are not overinfusing a patient when giving IV fluids also check the lung bases and urine output.
  • Lymph nodes. The lymph nodes are not palpable in health, and if the largest is  below .5cm in size and not growing then they are insignificant. Look for an infection in the area of drainage, a generalised inflammatory disease like miliary TB or infectious mononucleosis. Enlarged rubbery to hard LN are a result of primary or secondary malignancy. See if they are mobile and not attached to the skin or underlying tissues. If they are red and hot then an abcess is developing in them and if they are not warm but matted and tending to form a sinus or are discharging white chalky material then they have turned scrofulous and then look for evidence of TB in the discharge or from a biopsy at the edge of the ulcer. You should read up the genetic tests for tuberculosis. You should know the indications for a FNAC or an excision biopsy of the LN.
  • Thyroid. A non inflammatory, non-neoplastic enlargement of the thyroid is known as a goitre. The commonest cause of a goitre is iodine deficiency. This has become uncommon as most countries now add iodine supplements to salt in the diet. Puberty goiter is still commonly seen as the iodine requirement goes up. In addition to adding iodine to the salt a low dose of thyroxine will return the contour of the neck to normal as in young girls the cosmetic concern is the highest. Goitres can be nodular as multiple cysts develop in them. A single cyst specially if it shows evidence of increased circulation is usually evidence of hyperthyroidism. Thyroiditis can be associated with accelerated signs of hyperthyroidism or thyroid storm. Goitres can be associated with euthyroidism, hypothyroidism or hyperthyroidism. Tremors, palpitation, weight loss with an increased appetite and prominent eyes indicate hyperthyroidism. Atrial fibrillation may be a feature to look for. Lethargy, somnolence, weight gain, constipation and angina occur in hypothyroidism.
  • Hair: texture; normal hair is dry and springy. Flat hair which does not shine after washing indicates malnutrition specially protein malnutrition. Apart from starving children and refugees you will find it in patients with nephrotic syndrome. Baldness can be diffuse as after chemotherapy and in old age in women. Male type baldness occurs in young males and is usually genetic. It consists of temporal balding and loss of hair at the top of the skull. Elderly women may develop male type baldness. Patchy alopecia is always disease related and rarely treatable.
  • Skin eruptions. Many systemic illnesses leave their mark on the skin. Tumours such as neurofibromas, lipomata can be seen on the trunk, and limbs usually along nerves or tendons, Scratch marks and excoriation indicate severe pruritus from a dry skin, scabies or renal or hepatic disease. Sun sensitive pruritus and eruptions occur in SLE and porphyria cutanea tarda. Bruising and petechaie occur in low platelets and other bleeding disorders. Look for the eruption of herpes zoster along dermatomes supplied by nerves from one segment of the spinal cord. If you are looking for eruptions then look at the back, buttocks and back of the thighs because the patient cannot examine himself there. Diseases for which skin lesions are expected are : bullous SLE tense vesicles and blisters appear on normal-appearing or erythematous skin. In addition, rose-colored or red macules without overlying vesicles or bullae are often present. Erythema nodosum EN is a predominantly septal panniculitis without primary vasculitis . Early lesions will demonstrate septal edema with mild lymphocytic infiltrates, though neutrophils may be prevalent . A secondary vasculitis may be seen when there is a dense, mixed, or neutrophil-heavy inflammatory infiltrate. Concomitant thrombophlebitis may be present, particularly in cases associated with Behçet syndrome. There are many causes of EN like TB, Staphylococcus and streptococci infections. Remember some of the list.
  • Hands and nails. These can give a lot of information. First look at the colour; if the nails are paler than yours then there is anemia. Yellowness and cyanosis can also be seen there, iIn cyanotic congenital heart diseases, suppurative lung disease and carcinoma of the bronchus you may find clubbing. This is not a major finding to be looked for in every patient. Injured, broken and dirty nails indicate hard manual labor. The nails may be pitted or detached from the nail bed. There may be a pale band “leuconychia” in the nail bed indicating a period of hypoalbuminemiaAre there any tremors in the hand at rest or when the patient holds out his hands? Fine tremors occur in anxiety, fever, thyrotoxicosis and familial tremors. Coarse tremors at rest occur in Parkinson’s disease usually described as “pill rolling” tremors. Tremors at the end of a range of action are called “action tremors” are found in diseases of the cerebellum. Flapping of out stretched hands occur in chronic hepatic encephalopathy, advanced respiratory or renal failure.
  • Joints: look for arthritis, swelling, deformity of the big joints and joints of the fingers and toes. Look for tophi and joint abnormalities arising from damaged tendons. Note the pattern of distribution of involvement of the joints. Note any skin lesions like erythema marginatum or erythema multiforme.
  • Peripheral pulses. With advancing atherosclerosis and in diabetes peripheral pulses may become weak or disappear resulting in ischemia, non-healing ulcers and gangrene. Peripheral vascular disease can occur by itself. Diseases like Takayasu’s disease result in loss of pulses in the wrist and hand while the lower limb pulses are palpable. in acute emergencies embolisation of the femoral artery may occur and if not surgically corrected at once may result in the loss of a limb.
  • Ulcers on the soles of the feet, ankles and back. In chronic care wards and in critically ill the commonest non-healing ulcers are pressure sores (bed sore) or more correctly pressure injury. Pressure and shearing injury interfere with microvasculature, These are preventable if good nursing care is instituted at the start of the illness. These act as a source of infection which persists despite antibiotic therapy. in long-term care amyloidosis and squamous cell cancer may occur. In ambulatory patients loss of sensation contribute to injury and undue pressure on a spot leading to a non-healing ulcer. Loss of blood supply is a compounding factor.
  • Add up your findings and try to come to a logical conclusion.
  • Do a quick examination of the rest of the system to look for a pattern or group of signs. This is what the examiner means when he/she gives the command “Do the GPE and appropriate examination”.

Published by

shaheenmoin

I am a Professor of Medicine and a Nephrologist. Having served in the Army Medical College, Pakistan Army for 27 years I eventually became the Dean and Principal of the Bahria University Medical and Dental College Karachi from where I retired in 2016. My passion is teaching and mentoring young doctors. I am associated with the College of Physicians and Surgeons Pakistan as a Fellow and an examiner. I find that many young doctors make mistakes because they do not understand how they should answer questions; basically they do not understand why a question is being asked. My aim is to help them process the information they acquire as part of their education to answer questions, pass examinations and to best take care of patients without supervision of a consultant. Read my blog, interact and ask questions so that I can help you more.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s