Fig. 5D.50: Palpation of left kidney.

Fig. 5D.51: Palpation of right kidney.

Causes of unilateral and bilateral kidney enlargement:

Unilateral kidney enlargement Bilateral kidney enlargement

Renal cell carcinoma

Hydronephrosis

Polycystic kidneys

Bilateral hydronephrosis

Differences between spleen and left kidney

Characteristics Spleen Left kidney

Location Left hypochondrium Left lumbar

Direction of enlargement Towards RIF Towards left hypochondrium and LIF

Movement with respiration + –

Insinuation between left costal margin and organ Not possible Possible

Bimanual palpation – +

Ballotability – +

Crossing midline Can cross midline Never cross midline

Notch + –

Band of colonic resonance – +

Differences points between liver versus spleen versus kidney

Features Liver Spleen Kidney

Location Right

hypochondrium

Left

hypochondrium

Lumbar

Direction of enlargement Towards RIF Towards RIF Towards hypochondrium and iliac

fossa

Movement with respiration + + –

Insinuation of fingers between the costal margin

and organ

Not possible Not possible Possible

Bimanually palpable – – +

Ballotability – – +

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Anterior percussion Dull Dull Tympanic

Examination of Free Fluid in Abdomen

Ascites

Definition:

Ascites is defined as the accumulation of free fluid in the peritoneal cavity. The peritoneal cavity can

accumulate as much as 60 liters of fluid.

Massive ascites and tense ascites are the clinical terms and are described at the end.

Etiology of ascites

Nonperitoneal causes Peritoneal causes

Intrahepatic portal

hypertension

Cirrhosis

Fulminant hepatic failure

Veno-occlusive disease

Granulomatous

peritonitis

Tuberculous peritonitis

Fungal and parasitic

infections

Sarcoidosis

Foreign bodies (cotton,

starch, barium)

Extrahepatic portal

hypertension

Hepatic vein obstruction (i.e. Budd–

Chiari syndrome)

Congestive heart failure

Malignant ascites Primary peritoneal mesothelioma

Secondary peritoneal

carcinomatosis

Hypoalbuminemia Nephrotic syndrome

Protein-losing enteropathy

Malnutrition

Vasculitis Systemic lupus

erythematosus

Henoch-Schönlein purpura

Miscellaneous disorders Myxedema

Ovarian tumors

Pancreatic and biliary ascites

Miscellaneous

disorders

Eosinophilic gastroenteritis Whipple disease

Endometriosis

Chylous Secondary to malignancy, trauma

Serum-ascites albumin gradient (SAAG):

SAAG = (serum albumin)–(albumin level of ascitic fluid)

The serum-ascites albumin gradient (SAAG) is a better discriminant than older measures (transudate

versus exudate) for the causes of ascites.

The presence of a gradient ≥1.1 g/dL (≥11 g/L) predicts that the patient has portal hypertension with

97% accuracy.

High albumin gradient (SAAG ≥1.1 g/dL) Low albumin gradient (SAAG <1.1 g/dL)

Cirrhosis

Alcoholic hepatitis

Heart failure

Massive hepatic metastases

Heart failure/constrictive pericarditis

Budd–Chiari syndrome

Portal vein thrombosis

Idiopathic portal fibrosis

Peritoneal carcinomatosis

Peritoneal tuberculosis

Pancreatitis

Serositis

Nephrotic syndrome

Biliary ascites

Bowel obstruction

Bowel infarction

Ascites praecox:

It is defined as appearance of ascites before the generalized edema. It is usually associated with

chronic constrictive pericarditis.

Causes of ascites without significant edema:

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Chronic constrictive pericarditis

Tuberculous peritonitis

Malignant peritonitis

Pancreatic ascites

Acute Budd–Chiari syndrome.

Grading systems of ascites

The International Ascites Club grading (2003) Traditional system

Grade 1 Mild ascites detectable only by ultrasonography 1+ is minimal and barely detectable

2+ is moderate

3+ is massive but not tense

4+ is massive and tense

Grade 2 Moderate ascites manifested by moderate symmetrical abdominal distension

Grade 3 Large or gross ascites with marked abdominal distension

Following methods have been discussed of demonstration of ascites:

Fullness of flank

Horseshoe dullness

Shifting dullness

Fluid wave/fluid thrill

Puddle sign

Auscultatory percussion sign of Guarino.

Bulging flanks/fullness of flanks/horseshoe dullness

Occurs when the weight of abdominal free fluid is sufficient to push the flanks outward (Fig.

5D.52).

On inspection, it can be seen as fullness of flanks or bulging of flanks.

Bulging of flanks can be caused by ascites or by obesity.

One method for discriminating between the two is to test for flank dullness. With the patient recumbent, gas-filled loops of bowel will characteristically float on top of ascites, making the percussion note tympanic at the umbilicus and dull beyond the fluid meniscus into the

flanks—horseshoe dullness.

Fig. 5D.52: Horseshoe dullness.

Shifting dullness (Fig. 5D.53):

Presence of shifting dullness indicates at least 1.5 liters of free fluid in the peritoneal space.

Examination (Figs. 5D.54A to K):

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Patient in supine position, start percussion from above downwards in the midline, till below the

umbilicus you get dullness.

This dullness could be due to distended urinary bladder, hence repeat this after making the

patient empty the bladder.

Fig. 5D.53: Shift of dullness on lying in lateral decubitus position.

Figs. 5D.54A to H

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Figs. 5D.54I to K

Figs. 5D.54A to K: Demonstration of shifting dullness.

Now, begin by percussing at the umbilicus and moving toward the flanks.

The transition from air to fluid can be identified when the percussion note changes from tympanic

to dull.

Mark the dullness-tympany transition point.

Turn the patient to opposite lateral side and wait for 30–60 seconds.

Now percuss the area again.

The area of tympany will shift towards the top and the area of dullness shifts towards the bottom.

Repeat the same maneuver on the opposite side.

Causes of ascites without shifting dullness:

Massive ascites

Loculated ascites

Fluid thrill (fluid wave) assessment for ascites:

In supine position, ask the patient or an assistant to place the ulnar surface of one hand above

the umbilicus, pressing firmly (so the subcutaneous tissue and fat does not jiggle) with the hand

pointing towards the patient’s toes (Fig. 5D.55).

Use one hand to palpate and one hand to percuss.

Place a hand on the lateral aspect of the patient’s abdomen between the costal margin and the

ilium in the anterior axillary line.

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Fig. 5D.55: Demonstration of fluid thrill.

Tap one side of the patients flank sharply with your fingertips.

Feel on the opposite flank for an impulse transmitted through the fluid.

Repeat procedure by flicking on the other side.

Results:

Positive: An easily palpable impulse is felt on the opposite side of tapping suggesting ascites

of around more than 2 liters.

Negative: No impulse is felt.

False positive: Can be felt over large ovarian cyst or large hydatid cyst or large

hydronephrosis.

Puddle sign (Fig. 5D.57):

It is a sign of mild ascites of around 250 mL.

Not frequently done.

Patient is prone for 3–5 minutes and then examined in knee-elbow position as shown in the

Figure 5D.57.

Diaphragm of the stethoscope is placed over the most dependent area of the abdomen. Place

diaphragm of the stethoscope over the umbilical region and scratch the abdominal wall from

periphery to umbilicus.

Sudden change in the note is a positive sign.

Sign can be false positive in case of massive splenomegaly or distended urinary bladder.

Auscultatory percussion (described by Guarino)

After voiding, the patient sits or stands so that free fluid gravitates to the pelvis, and the examiner

places a stethoscope in the midline, immediately above the pubic crest.

Finger-flicking percussion is performed along radial spokes from the subcostal margin downward

toward the pelvis.

The percussion note is initially dull but changes sharply to a loud note at the border of increased

pelvic density.

In the absence of ascites, the border is approximately 4.5 cm above the pelvic crest (the pelvic

baseline).

In patients with ascites, free fluid raises the demarcating border clearly above the pelvic baseline. When the patient is supine, this clear line of demarcation is obliterated because the free fluid

gravitates to the flanks.

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The sensitivity, specificity, and likelihood ratio of different methods of examination of ascites:

Method Amount of fluid LR+ LR- Sn Sp

Fullness of flanks 2.0 0.3 0.81 0.59

Horseshoe dullness 2.0 0.3 0.84 0.59

Shifting dullness 1.5 liters 2.7 0.3 0.77 0.72

Fluid thrill > 2 liters 6.0 0.4 0.62 0.9

Puddle sign 250 mL 1.6 0.8 0.45 0.73

What is tense ascites and massive ascites?

The earliest clinical sign of ascites is puddle sign which is positive with as low as 250 mL of ascitic

fluid.

Shifting dullness is a specific sign of ascites which occurs due to the floating of the bowel loops in

ascitic fluid. This appears when the fluid accumulation is around 1.2 liters.

As the fluids accumulate further, fluid thrill appears (at around 2 liters). Appearance of fluid thrill

makes the ascites tense.

As the ascitic fluid fills, the mesentery is stretched and bowel loops float in the ascitic fluid. As the

mesentery can only stretch up to a limit, further fluid accumulation results in the submersion of bowel

loops. At this stage, shifting dullness disappears; however, fluid thrill persists (Fig. 5D.56). This

condition is called as massive ascites.

Fig. 5D.56: Schematic representation showing relationship between shifting dullness and fluid thrill with

respect to increasing ascites.

Diagrammatic representation of signs of ascites (Fig. 5D.57):

Examination of Dilated veins

Position of Patient

Make the patient stand and examine the anterior abdominal wall, the flanks, and back for dilated veins.

Dilated tortuous veins are significant.

Steps of examination (Harvey’s sign) (Figs. 5D.58A to D):

The direction of blood flow in the veins is examined by placing the tips of the index fingers together

and compressing the vein.

Then, the finger tips are slid apart producing an empty segment of the vein between the fingers (Fig.

5D.59A).

Then, one finger is removed and filling of the vein is observed (Fig. 5D.59B).

The procedure is repeated but, now the opposite finger is removed and filling is observed (Fig.

5D.59C).

The direction of flow of the veins is the direction in which the filling was rapid and more.

Fig. 5D.57: Signs of ascites.

Figs. 5D.58A to D: Harvey’s sign.

Condition (Fig. 5D.60) Direction of flow in veins above

umbilicus

Direction of flow in veins below

umbilicus

Normal (veins not visible) Upwards Downwards

Portal hypertension (veins are visible and

tortuous)

Upwards Downwards

Portal vein thrombosis Downwards Upwards

Superior vena cava (SVC) obstruction Downwards Downwards

Inferior vena cava (IVC) obstruction Upwards Upwards

Note: Caput medusa: Dilated tortuous veins around the umbilicus resembling the head of medusa.

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Figs. 5D.59A to C: (A) The finger tips are slid apart producing an empty segment of the vein between

the fingers; (B) One finger is removed and filling of the vein is observed; (C) Procedure is repeated but,

now the opposite finger is removed and filling is observed.

Fig. 5D.60: Direction of flow of veins.

Per-Rectal Examination

Rectal examination consists of:

Visual inspection of the perianal skin

Digital palpation of the rectum

Assessment of neuromuscular function of the perineum.

Preferred position of examination:

The lateral decubitus, or Sims position, provides optimal examination. The patient lies on the left side

with the buttocks near the edge of the examining table or bedside with the right knee and hip in slight

flexion.

The rectal examination involves both inspection and palpation. First, using a gloved hand, the

examiner inspects the buttocks for fistulous tracts, the skin tags, excoriations, blood, fissures in patients

with inflammatory bowel disease, rectal prolapse, and superficial ulcers.

Palpation of the rectum can reveal ulcers, masses.

Tenderness may be felt with prostatitis, pelvic inflammatory disease, tubo-ovarian abscesses,

ovarian cysts, ectopic pregnancy, and inflammatory bowel disease.

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Also note the consistency, color, and presence of frank or occult blood in the stool (melena). Black

stools result from degraded blood (melena), iron, licorice, bismuth, rhubarb, or overindulgence in

chocolate cookies. Red-colored stools may be due to brisk bleeding known as hematochezia (usually

distal to the ligament of Treitz).

Hemorrhoids are usually not felt unless thrombosed. Proctoscopy is the best way to look for

hemorrhoids.

Others

Per vaginal/per speculum examination—

In female patients with ascites, ovarian neoplasms, pelvic tumor, per vaginal mass/bleeding can be

detected.

GIT examination is incomplete without examination of the three S’s; Scrotum, Spine, and

Supraclavicular Fossa

Scrotum—hydrocele, hernia, testicular atrophy, and testicular tumors

Spine—metastasis and Pott’s spine

Supraclavicular fossa—metastasis to left scalene node.

COMPLICATIONS OF CIRRHOSIS

Table 5D.1 represents complications of cirrhosis.

Table 5D.1: Complications of cirrhosis.

Portal hypertension and its

sequelae

Hepatic encephalopathy Hepatocellular carcinoma

Ascites Portal gastropathy Bleeding manifestations and

coagulopathy

Spontaneous bacterial peritonitis Hepatorenal syndrome Cirrhotic cardiomyopathy

Portopulmonary hypertension Hepatopulmonary syndrome Hepatic hydrothorax

Coagulopathy,

thrombocytopenia,

Hyponatremia

Endocrine dysfunction—adrenal insufficiency, gonadal

dysfunction, and thyroid dysfunction

Cirrhotic osteodystrophy

Hepatic Encephalopathy

Types of Hepatic Encephalopathy (Fig. 5D.61):

West Haven criteria clinical grade of hepatic encephalopathy

Grade Description Asterixis

Grade

0/Minimal

HE

Lack of detectable changes in personality or behavior Absent

Grade 1 Trivial lack of awareness, euphoria or anxiety, shortened attention span, impaired performance of

addition

May be

present

Grade 2 Lethargy or apathy, minimal disorientation for time or place, subtle personality change, inappropriate

behavior, slurred speech, impaired performance of subtraction

Present

Grade 3 Somnolence to semi-stupor, but responsive to verbal stimuli, confusion, gross disorientation Usually

absent

Grade 4 Coma (unresponsive to verbal or noxious stimuli) –

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Fig. 5D.61: Types of hepatic encephalopathy.

Asterixis:

Described earlier in signs of liver cell failure.

Diagnosis of Minimal Hepatic Encephalopathy

It is currently based on neuropsychometric tests, including the number connection test, digit symbol test,

and the block design test.

Reitan’s number-connection test (Fig. 5D.62):

There are 25 numbered circles which can normally be joined together within 30 seconds.

Hepatorenal Syndrome

Diagnostic criteria for hepatorenal syndrome

All of the following must be present for the diagnosis of hepatorenal syndrome (HRS)

Cirrhosis with ascites

Serum creatinine >1.5 mg/dL

No improvement of serum creatinine (decrease to a level of 1.5 mg/dL or less) after at least 2 days of diuretic withdrawal and

volume expansion withalbumin

Absence of shock

No current or recent treatment with nephrotoxic drugs

Absence of parenchymal kidney disease as indicated by proteinuria >500 mg/day, microhematuria (>50 red blood cells per high

power field), and/or abnormal renal ultrasonography

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