Showing posts with label Clinical examination. Show all posts
Showing posts with label Clinical examination. Show all posts

Monday, November 30, 2015

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BMI versus waist to hip ratio

 DEFINITION 
Obesity is a state of excess adipose tissue mass. It is often viewed as equivalent to an increased body weight. This is not true because muscular individuals may have increased body weight but are not obese.

Weight follows a continuous distribution pattern in human population. The point at which mortality and morbidity becomes statistically significant is the cut-off to call a patient obese.

 METHODS 
Various methods have been used to measure obesity. These include:
1) Anthropometry (skin-fold thickness)
2) Densitometry (underwater weighing)
3) CT/MRI
4) Electrical impedance.

Still the most common techniques used in clinical practice are:
1) BMI measurement
2) Waist-to-hip ratio measurement.

 BMI 
It is not an accurate measure of obesity but since it is simple to calculate, it is the most frequently measured parameter.

At similar BMI, women usually have more fat than men. When the BMI > 25 Kg/m2, morbidity starts to increase and if associated with risk factors then therapeutic interventions should be considered.



 WAIST-TO-HIP RATIO (WHR) 
Intra-abdominal or abdominal subcutaneous tissue fat has more significant implications on morbidity than fat present in the buttocks and lower extremities. A WHR > 0.9 for women and > 1.0 for men is considered abnormal. (0.85 and 0.90 respectively according to WHO)

Insulin resitance, hypertension, dyslipidemia and diabetes mellitus are more strongly associated with intra-abdominal / abdominal subcutaneous tissue fat than to overall adiposity.

The probable explanation of this issue is that intra-abdominal adipocytes may be lipolytically more active than those from other depots. There is also release of free fatty acids into the portal circulation and this has adverse metabolic effects, especially on the liver.

A recent article published in the Annals of Internal Medicine concluded that
" normal-weight U.S. adults with central obesity have the worst long-term survival compared with participants with normal fat distribution, regardless of BMI category, even after adjustment for potential mediators. "

First published on: 30 November 2015

Monday, March 9, 2015

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kussmaul breathing pattern - description and causes

This type of breathing pattern was first described by Adolph Kussmaul, a german physician in 1874. He noticed that his patients with diabetic ketoacidosis had a pattern of breathing which he first labelled as having "air hunger".

In the Kussmaul type of breathing, the patient is breathing heavily i.e hyperventilating along with tachypnea.
So we will find that the amplitude of the breaths along with the rate will be increased.
There is usually no pauses between the breaths.

This is not specific for diabetic ketoacidosis. It can also appear in other types of severe metabolic acidoses e.g alcoholic ketoacidosis .

Sunday, October 14, 2012

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Edema - Definition, pathophysiology, causes, clinical features


 DEFINITION 
Edema is an abnormal presence of excessive fluid in the interstitial space.

 PATHOPHYSIOLOGY 
The movement of water and low molecular weight solutes such as salts between the intravascular and interstitial spaces is controlled primarily by the opposing effect of vascular hydrostatic pressure and plasma colloid osmotic pressure. Normally the outflow of fluid from the arteriolar end of the microcirculation into the interstitium is nearly balanced by inflow at the venular end. A small residual amount of fluid may be left in the interstitium and is drained by the lymphatic vessels, ultimately returning to the bloodstream via the thoracic duct.


Either increased capillary pressure, diminished colloid osmotic pressure or inadequate lymphatic drainage can result in an abnormally increased interstitial fluid i.e. edema. An abnormal increase in interstitial fluid within tissues is called edema, while fluid collections in the different body cavities are variously designated hydrothorax (pleural cavity), hydropericardium (pericardial cavity) and hydroperitoneum (the last is more commonly called ascites). Anasarca is a severe and generalized edema with widespread subcutaneous tissue swelling.


The diagram above shows the actual change in pressure gradients at the capillary level. The numbers represent the pressure in the vessels in mmHg.
At the arteriolar end, the hydrostatic pressure (outward force) is 37 mmHg while the oncotic pressure and interstitial pressure (inward forces) are 25 and 1 mmHg respectively. Thus the net outward force is 37 – (25+1) = +11 mmHg. Since the net outward force is positive fluid moves from the capillary to the interstitial spaces.
At the venular end, the hydrostatic pressure is lower and has a value of 17 mmHg. The oncotic and interstitial pressure on the other hand remain the same i.e. a total of 26 mmHg (25+1). Thus the net outward force is 17 – (25+1) = -9 mmHg. Since the outward force is negative, it means fluid is not getting out of the capillary but instead it is moving into it.

The arrows in the diagram show the magnitude and direction of net fluid movement.

 CLASSIFICATION  
1) According to pathophysiological mechanism:
                a) Transudate (low protein content)
                b) Exudate (high protein content)
2) According to location:
                a) Localized
                b) Generalized
3) According to clinical finding:
                a) Pitting
                b) Non-pitting.

 LOCALIZED EDEMA 
It means that the edema is localized to a specific region of the body. It is commonly due to venous/lymphatic causes, allergy and inflammation.

1) Venous edema: It is due to high venous pressure or venous constriction. Intravascular venous obstruction e.g. Deep vein thrombosis (DVT) or an external compression like a mass (tumour) or plaster are the common causes but there can also be failure of venous pumps due to paralysis of muscles (Cerebro-vascular accident), immobilization of parts of the body (Post-op, fractures) and failure of venous valves (Varicose veins). It is more frequent to see localized edema in the lower limbs but the upper limbs may also be affected.

2) Lymphatic edema: It is due to a blockage in the lymphatic return. It commonly occurs in conditions like cancer/ post-radiation, infections like elephantiasis (Filaria nematodes), surgery or congenital absence or abnormality of lymphatic vessels. The edema is persistent and non-pitting type. In case of elephantiasis, the affected limb may be dramatically enlarged.

3) Allergy/Angioedema (Quincke edema): During a case of allergy there is release of histamine and other mediators that lead to vasodilation. The swelling can involve the face, lips, tongue and even glottis. Edema of the glottis is a medical emergency as it can lead to asphyxia if not treated quickly. This type of edema is usually itchy but transitory. It resolves with antihistaminics and steroids.

4) Inflammation: Here also there is vasodilation because of the inflammatory mediators. Edema is seen with superficial (cellulitis) or deep infections (abscess).

 GENERALIZED EDEMA 
In this case the edema involves more than 1 part of the body simultaneously. It is commonly due to cardiac, hepatic, renal or endocrine causes.

1) Cardiac edema: The initial pathology is because of increased venous pressure but as the condition becomes more severe, there is impairment of renal blood supply, activation of rennin-angiotensin-aldosterone system and finally hypoalbuminemia secondary to liver stasis. Left sided heart failure leads to pulmonary edema while right sided heart failure causes peripheral edema, ascites, hydrothorax and anasarca in severe and long standing cases. The edema is progressive. In ambulant individuals, it moves up with severity. The edema is usually of pitting type. In early stages of heart failure, there is improved renal circulation at night leading to nycturia. Thus the edema will be less in the morning and progressively increases towards the end of the day.

2) Hepatic edema: Liver pathology like cirrhosis leads to decreased synthesis of proteins. The hypoalbuminemia leads to decreased oncotic pressure. The scarred liver also causes a back pressure in the portal vein territory (portal vein hypertension) and increases the hydrostatic pressure there. These 2 factors combined lead to edema in the peritoneal cavity (ascites) and this in turn compresses the inferior vena cava and leads to edema in the lower limbs.

3) Renal edema: Kidney diseases like nephritic syndrome with decreased glomerular filtration rate and sodium/water retention or nephrotic syndrome where there is albumin loss in the urine lead to generalized edema. The edema frequently occurs in lax connective tissue like the face, periorbital area and genitalia. It is of pitting type. It occurs mostly during the morning and is associated with vasoconstriction. Thus it is called as ‘white’ edema.

4) Endocrine edema: Many endocrine problems can cause edema. In case of hyperaldosteronism (primary or secondary), there is retention of sodium and water. This leads to an increase in hydrostatic pressure. The edema is of pitting type. On the other hand, myxedema refers to a non-pitting type of edema seen in hypothyroidism. Finally, females experience edema as part of the pre menstrual syndrome due to hormonal changes.

 CAUSES OF EDEMA (ACCORDING TO PATHOPHYSIOLOGY) 
  1. Increased capillary pressure (increased hydrostatic pressure)
    1. Excessive kidney retention of salt and water
      1. Acute or chronic kidney failure
      2. Mineralocorticoid excess
    2. High venous pressure and venous constriction
      1. Impaired heart functioning (Congestive heart failure, constrictive pericarditis)
      2. Venous obstruction (Deep vein thrombosis, External compression like a mass or plaster)
      3. Failure of venous pumps
        • (a) Paralysis of muscles (Cerebro-vascular accident)
        • (b) Immobilization of parts of the body (Post-op, fractures)
        • (c) Failure of venous valves (Varicose veins)
    3. Decreased arteriolar resistance
      1. Excessive body heat
      2. Insufficiency of sympathetic nervous system
      3. Drugs (vasodilators, calcium channel blockers)
  2. Decreased plasma proteins
    1. Loss of proteins in urine (Nephrotic syndrome) or G.I.T (Protein-losing gastroenteropathy)
    2. Loss of protein from denuded skin areas
      1. Burns
      2. Wounds
    3. Failure to produce proteins
      1. Liver disease (Cirrhosis)
      2. Serious protein or caloric malnutrition
  3. Increased capillary permeability
    1. Immune reactions that cause release of histamine and other immune products (Allergy)
    2. Toxins
    3. Bacterial infections (Cellulitis)
    4. Vitamin deficiency, especially vitamin C
    5. Prolonged ischemia
    6. Burns
  4. Blockage of lymph return
    1. Cancer
    2. Infections (Filaria nematodes)
    3. Surgery
    4. Congenital absence or abnormality of lymphatic vessels
    5. Post-radiation.
 CLINICAL FEATURES 
In dependent edema, which is typically present in congestive heart failure and in conditions associated with a low plasma protein level, the swelling first appears at the ankles and over the dorsum of the foot and only gradually involves the legs, thighs and trunk. The best place to check for slight degrees of edema in an ambulant patient is behind the malleoli at the ankles. In bed-bound patients edema often appears first over the sacrum. To recognize pitting edema it is important to press firmly and for a sustained period of 20-30s over a bony prominence (tibia, lateral malleoli or sacrum) to provide effective compression. The 'pit' will be as easily felt as seen. If the finger pressure is not maintained for an adequate period of time then slight degrees of edema may be overlooked.

Edema can be recognized by the pallid and glossy appearance of the skin over the swollen part, by its doughy feel and by the fact that it pits on finger pressure.
The edema of lymphatic obstruction does not pit on pressure or there may be minimal pitting. The skin is usually thickened and tough.

 N.B 
1) Without redness and scaling, bilateral periorbital edema may indicate acute nephritis, nephrosis or trichinosis. If there is irritation, contact dermatitis is the probable diagnosis.
2) In local venous obstruction the edema is confined to the parts from which the return of blood is impeded. Local edema is sometimes seen over inflamed joints.
3) Edema of the whole upper part of the body may result from intrathoracic tumours.

Last reviewed on: 1 September 2015





Sunday, May 20, 2012

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Abdominal examination - liver


Liver
Examination sequence:
1) Start the palpation in the right iliac fossa. If you start in the right lumbar or right hypochondrium you may miss a massively enlarged liver.
2) The radial border of the right hand is used to feel the liver. The hand must be placed flat on the abdomen. Make sure you do not poke the patient’s abdomen with your finger tips.
3) Now your right hand is kept stationary and the patient is asked to take a deep breath. During inspiration the diaphragm becomes flat and pushes the liver downwards. Try feeling the edge when the patient inspires.
4) As the patient breathes out, move your hand up the abdomen for 1-2cm. Step 3) is then repeated.
5) Repeat step 4) till you reach the costal margin or you detect the edge of the liver.
6) If you feel the edge, then you have to work out whether it is a true enlargement of the liver or the latter has been displaced downwards by a hyperinflated lung e.g. in a case of emphysema. To check this, you have to percuss the lung on the right hemithorax. The lower 3-4 intercostal spaces are usually dull to percussion. If resonant then it is most probably a hyperinflated lung.
7) If true enlargement is concluded then measure the distance below the costal margin in the midclavicular line in cm.

Another way to perform the examination is:
1)  Place both of your hands side by side flat on the abdomen in the right iliac fossa lateral to the rectus muscles with the fingers pointing towards the ribs. Feel the edge of the liver with the pulp of your fingers, not your nails.
2) Repeat steps 3) to 7) as above but using the two hands side by side method.

Other method, like using the left hand at the back and palpating using the right hand in front, is also commonly used but it is less accurate.

Now if you have an enlarged liver you have to describe it in terms of:
a) Surface – smooth or irregular
b) Edge – smooth or irregular
c) Consistency – soft, firm or hard
d) Tenderness
e) Pulsatile
f) Audible bruit.

Causes of hepatomegaly:
1) Chronic parenchymal liver diseases like alcoholic liver disease, autoimmune hepatitis, viral hepatitis, primary biliary cirrhosis. Hepatic enlargement occurs mainly at the beginning of the diseases. Later on, due to fibrosis, it shrinks. In these conditions the liver is usually firm in consistency and regular surface.
2) Malignancy which can be primary hepatocellular cancer or secondary metastatic cancer. In hepatocellular cancer, an audible bruit may be heard while metastatic deposits give an irregular surface (sometimes nodular) with hard consistency but without tenderness.
3) Right sided heart failure in which the lung will be soft in consistency and can be tender.  If the failure is due to tricuspid regurgitation then we can feel a pulsatile liver.
4) Hematological disorders like lymphoma, leukemia, polycythemia and myelofibrosis.
5) Rare cases like amyloidosis, Budd-Chiari syndrome and glycogen storage disorders.

Note:
1) Always request the patient to flex the knees before the examination in order to relax the abdominal wall.
2) Normal length of liver in midclavicular line is <12 cm. Mean length for women=7 cm, men= 10.5 cm.
3) Single handed palpation is better for lean individual while bimanual for obese/muscular individuals.
4) Normal liver is palpable in the cases of emphysema as mentioned above but also if there is a right-sided pleural effusion, Riedel’s lobe or deep diaphragmatic excursion.

Liver disease
Palpation
Size
Acute hepatitis
Smooth; surface tender
Enlarged
Chronic hepatitis
Firm liver edge
Enlarged, especially left lobe
Nodules rare; tender
Fulminant hepatitis
Tender surface
Shrinking size
Cirrhosis
Non-tender, firm
Variable; late stages, liver decreases in size
Hepatocellular carcinoma (hepatoma)
Nodules, if present, large and hard
Moderate to massive enlargement
Non-tender
Metastatic carcinoma
Large nodules, irregular surface
Enlarged
Non-tender
Fatty liver
Smooth surface
Enlarged
Right heart failure
Soft, smooth, tender
Mild to massive enlargement