Guarding

Rigidity

Deep palpation

Liver

Size

Shape

Border or edge

Surface

Tenderness

Consistency

Movement with respiration

Pulsation

Spleen

Location

Size

Shape

Consistency

Surface

Edge

Tenderness

Movement with respiration

Gallbladder

Other palpable mass

Bimanual palpation

Kidneys

Location

Size

Shape

Consistency

Surface

Edge

Tenderness

Movement with respiration

Dipping method (in case of large ascites)

Hernia orifices

Direction of flow in veins (if dilated veins present)

Abdominal girth measurement

Spino-umbilical distance

Xiphisternum to umbilicus distance (x) in cms

Umbilicus to pubic symphysis distance in cms (y)

Ratio of x/y

Percussion:

Liver

Spleen

Traube’s space

Fluid

Shifting dullness

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Fluid thrill

Puddle sign

Auscultation:

Bowel sounds

Succussion splash

Bruit

Venous hum

Friction rub

Examination of

Scrotum

Spine

Supraclavicular fossa

Per Rectal Examination

Per Vaginal Examination

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B. DIAGNOSIS FORMAT

CIRRHOSIS/LIVER DISEASE

Acute hepatitis <4 weeks

or

Subacute hepatitis

or

Chronic (cirrhosis/hepatitis >6 months)

or

Acute on chronic liver disease (ACLD)

Compensated or decompensated

Possible etiology—alcohol/postviral/toxin/nonalcoholic steatohepatitis (NASH)

With complications—portal hypertension with or without gastrointestinal (GI) bleed/hepatic

encephalopathy (preferable to mention stage)/spontaneous bacterial peritonitis/hepatocellular

carcinoma/hepatorenal syndrome/others.

EXAMPLE

Decompensated chronic liver disease—cirrhosis secondary to alcohol, with portal hypertension, with

upper gastrointestinal (UGI) bleed, patient in stage 2 hepatic encephalopathy with no evidence of

spontaneous bacterial peritonitis or other complications.

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C. DISCUSSION ON CARDINAL SYMPTOMS

ABDOMINAL SWELLING

Abdominal swelling is a manifestation of numerous diseases. Patients may complain of bloating or

abdominal fullness. Patients with abdominal distension from ascites may report the new onset of an

inguinal or umbilical hernia. Dyspnea may result from pressure against the diaphragm.

Causes

The causes of abdominal swelling can be remembered conveniently as the seven Fs: flatus, fat, fluid,

fetus, feces, full bladder, or a “fatal growth”/neoplasm.

Flatus The normal small intestine contains ∼200 mL of gas made up of nitrogen, oxygen, carbon dioxide,

hydrogen, and methane

Aerophagia, the swallowing of air, can result in increased amounts of oxygen and nitrogen in the small

intestine and lead to abdominal swelling

Increased intestinal gas is the consequence of bacterial metabolism of excess fermentable substances

such as lactose and other oligosaccharides, which can lead to production of hydrogen, carbon dioxide, or methane

Fat Weight gain with an increase in abdominal fat can result in an increase in abdominal girth

Visceral obesity is associated with metabolic syndrome, insulin resistance, and cardiovascular disease

It also can be a manifestation of certain diseases, such as Cushing’s syndrome

Fluid The accumulation of fluid within the abdominal cavity (ascites) often results in abdominal distension

Fetus Pregnancy results in increased abdominal girth. Typically, an increase in abdominal size is first noted at 12–

14 weeks of gestation, when the uterus moves from the pelvis into the abdomen

Feces In the setting of severe constipation or intestinal obstruction, increased stool in the colon leads to increased

abdominal girth. These conditions are often accompanied by abdominal discomfort or pain, nausea, and

vomiting and can be diagnosed by imaging studies

Fatal

growth/neoplasm

An abdominal mass can result in abdominal swelling. Neoplasms, abscesses, or cysts can grow to sizes that

lead to increased abdominal girth. Enlargement of the intra-abdominal organs, specifically the liver

(hepatomegaly) or spleen (splenomegaly), or an abdominal aortic aneurysm can result in abdominal

distension

Full bladder Bladder distension also may result in lower abdominal swelling. It will be associated with anuria

JAUNDICE

Discussed in detail in Chapter 2C: Physical Examination.

GASTROINTESTINAL BLEEDING

Gastrointestinal bleeding (GIB) presents as either overt or occult bleeding.

Overt GIB Occult GIB

Overt GIB is manifested by hematemesis, vomitus of red

blood, or “coffee-grounds” material; melena, black, tarry

stool; and/or hematochezia, passage of red or maroon blood

from the rectum

Occult GIB may present with symptoms of blood loss or anemia,

such as lightheadedness, syncope, angina, or dyspnea; or with

iron deficiency anemia or a positive fecal occult blood test on

routine testing

GIB is also categorized by the site of bleeding as:

UGIB (esophagus, stomach, and duodenum)

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LGIB (colonic), small intestinal, or obscure GIB (if the source is unclear).

Hematemesis is the vomiting of blood, which may be obviously red or have an appearance similar to

coffee grounds.

Melena is the passage of black, tarry stools due to altered blood (blood should remain in the gut for 14

hours approximately). It usually means bleeding episodes from sites above the ligament of Treitz.

However, even up to middle of transverse colon can produce melena. It takes 60 mL or more of blood in

the stomach to turn stools black. One episode of bleed can produce 5–7 episodes of melena.

Hematochezia is the passage of fresh blood per anus, usually in or with stools.

Upper Gastrointestinal Sources of Bleeding

Causes

Esophageal causes Gastric causes Duodenal causes

Esophageal varices

Esophagitis

Esophageal cancer

Esophageal ulcers

Malory–Weiss tear

Gastric ulcer

Gastric cancer

Gastritis

Gastric varices

Dieulafoy’s lesions

Gastric antral vascular ectasia

Portal hypertensive gastropathy

Duodenal ulcer

Vascular malformations including aortoenteric fistulae

Hemobilia or bleeding from biliary tree

Hemosuccus pancreaticus or bleeding from the pancreatic duct

Severe superior mesenteric artery syndrome

Lower Gastrointestinal Bleeding (Fig. 5C.1)

Causes of LGI bleeding

Colonic bleeding (95%) Small intestinal bleeding (5%)

Diverticular disease Angiodysplasia

Anorectal disease (hemorrhoid, anal fissure, fistula in ano, solitary rectal ulcer, etc.) Crohn’s disease and infectious disease

Neoplasia (polyp, ulcerated lesions) Neoplasia (polyp, ulcerated lesions)

Inflammatory bowel disease Radiation

Infectious collitis

Angiodysplasia Meckel’s diverticulum

Radiation collitis/proctitis Aortoenteric fistula

Other Mesenteric ischemia

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Fig. 5C.1: Lower gastrointestinal bleeding.

NAUSEA AND VOMITING (TABLE 5C.1)

Definitions

Nausea is the subjective feeling of a need to vomit. Vomiting (emesis) is the oral expulsion of

gastrointestinal contents due to gut and thoracoabdominal wall contractions.

Mechanism of Initiation of Emesis

Brainstem nuclei—including the nucleus tractus solitarius; dorsal vagal and phrenic nuclei; medullary

nuclei regulating respiration; and nuclei that control pharyngeal, facial, and tongue movements—

coordinate initiation of emesis involving neurokinin NK1, serotonin 5-HT3, and vasopressin pathways.

Clinical Clues for Diagnosis

Gastroparesis and pyloric obstruction elicit vomiting within an hour of eating.

Emesis from intestinal blockage occurs later.

Vomiting occurring minutes after meal consumption prompts consideration of rumination syndrome. With severe gastric emptying delays, the vomitus may contain food residue ingested days before.

Feculent emesis is noted with distal intestinal or colonic obstruction.

Bilious vomiting excludes gastric obstruction, whereas emesis of undigested food is consistent with a

Zenker’s diverticulum or achalasia.

Vomiting can relieve abdominal pain from a bowel obstruction, but has no effect in pancreatitis or

cholecystitis.

Profound weight loss raises concern about malignancy or obstruction.

An intracranial source is considered if there are headaches or visual field changes.

Vertigo or tinnitus indicates labyrinthine disease.

Projectile vomiting is a type of severe vomiting in which stomach contents are forcefully propelled

several feet away from the patient and is usually not associated with nausea. It is a classical feature of

raised intracranial tension.

DIARRHEA

Definitions

Diarrhea is loosely defined as passage of abnormally liquid or unformed stools at an increased

frequency. For adults on a typical Western diet, stool weight >200 g/d can generally be considered as

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diarrhea.

Diarrhea may be further defined as acute if <2 weeks, persistent if 2–4 weeks, and chronic if >4

weeks in duration.

Table 5C.1: Causes of nausea and vomiting.

Intraperitoneal Extraperitoneal Medications/Metabolic disorders

Obstructing disorders

Pyloric obstruction

Small bowel obstruction

Colonic obstruction

Superior mesenteric artery syndrome

Enteric infections

Viral

Bacterial

Inflammatory diseases

Cholecystitis

Pancreatitis

Appendicitis

Hepatitis

Altered sensorimotor functions

Gastroparesis

Intestinal pseudo-obstruction

Gastroesophageal reflux

Chronic nausea vomiting syndrome

Cannabinoid hyperemesis syndrome

Rumination syndrome

Biliary colic

Abdominal irradiation

Cardiopulmonary disease

Cardiomyopathy

Myocardial infarction

Labyrinthine disease

Motion sickness

Labyrinthitis

Intracerebral disorders

Malignancy

Hemorrhage

Abscess

Hydrocephalus

Psychiatric illness

Anorexia and bulimia nervosa

Depression

Postoperative vomiting

Drugs

Cancer chemotherapy

Antibiotics

Antiarrhythmic drugs

Digoxin

Oral hypoglycemic agents

Oral contraceptives

Antidepressants

Anti-Parkinson’s agents

Smoking cessation agents

Endocrine/metabolic disease

Pregnancy

Uremia

Ketoacidosis

Thyroid and parathyroid disease

Adrenal insufficiency

Toxins

Ethanol

Types of Diarrhea

Inflammatory diarrhea is characterized by frequent, small-volume, bloody stools and may be

accompanied by tenesmus, fever, or severe abdominal pain. Inflammatory diarrhea is suspected with

the demonstration of leukocytes or leukocyte proteins (e.g. calprotectin or lactoferrin) on stool

examination.

Fatty stools are suggested by a history of weight loss, greasy or bulky stools that are difficult to

flush, and oil in the toilet bowl that requires a brush to remove. Floating stools indicate gas

production by colonic bacteria, not steatorrhea. Watery diarrhea can be further classified as osmotic or secretory in origin. Osmotic diarrhea is due

to the ingestion of poorly absorbed ions or sugars. Secretory diarrhea is due to disruption of

epithelial electrolyte transport.

Large-volume versus small-volume diarrhea

Large-volume diarrhea Small-volume diarrhea

Right colonic or small bowel disorders Left colonic disorders

The rectosigmoid reservoir is intact Compromises the rectosigmoid reservoir capacity

Individual bowel movements are less frequent and larger Frequent small-volume bowel movements

Normal rectosigmoid colon functions as a storage reservoir.

Acute diarrhea Chronic diarrhea

More than 90% of cases of acute diarrhea are caused by infectious agents;

these cases are often accompanied by vomiting, fever, and abdominal pain.

The remaining 10% are caused by medications, toxic ingestions, ischemia,

food indiscretions, and other conditions (Table 5C.2)

Diarrhea lasting >4 weeks warrants evaluation to

exclude serious underlying pathology. In contrast

to acute diarrhea, most of the causes of chronic

diarrhea are noninfectious (Table 5C.3)

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Table 5C.2: Causes of acute diarrhea.

Viral infection Viral gastroenteritis; Norovirus or rotavirus

Bacterial infection Campylobactor, Escherichia coli, Salmonella or shigella

Parasitic infection Cryptosporidium, Entamoeba histolytica or giardia

Traveler’s diarrhea Consuming food or drinks contaminated with bacteria, parasites or viruses

Medication Antibiotics and long-term use of proton pump inhibitors, increased risk of Clostridium difficile

infections

Food allergy or

intolerance

Cow’s milk, egg, seafood, soy or fructose or lactose intolerance

Digestive disorder Celiac disease, Crohn’s disease, irritable bowel syndrome or ulcerative colitis

Artificial sweetener Mannitol, sorbitol or xylitol found in sugar-free candies or gums

Table 5C.3: Causes of chronic diarrhea.

Fatty diarrhea Watery diarrhea

Malabsorption syndromes:

Mucosal diseases, (e.g.,

celiac disease, Whipple’s

disease)

Mesenteric ischemia

Short bowel syndrome

Small intestinal bacterial

growth.

Maldigestion:

Inadequate luminal bile acid

concentration

Pancreatic exocrine

insufficiency

Inflammatory diarrhea

Diverticulitis

Infectious diseases:

Invasive bacterial infections

(e.g. tuberculosis and

yersiniosis)

Invasive parasitic infections

(e.g. amebiasis and

strongyloidiasis)

Pseudomembranous colitis

(Clostridium difficile

infection)

Ulcerating viral infections

(cytomegalovirus, herpes

simplex virus).

Inflammatory bowel diseases:

Crohn’s disease, ulcerative

colitis

Ischemic colitis

Neoplasia: carcinoma of colon,

lymphoma

Radiation colitis

Osmotic diarrhea:

Carbohydrate malabsorption

Osmotic laxatives

Secretory diarrhea

Bacterial toxins

Congenital syndromes (e.g. congenital chloridorrhea)

Disordered motility, regulation:

Diabetic autonomic neuropathy

Irritable bowel syndrome

Postsympathectomy diarrhea

Postvagotomy diarrhea

Diverticulitis

Endocrinopathies: Addison’s disease, carcinoid syndrome, gastrinoma, hyperthyroidism, mastocytosis, medullary carcinoma of thyroid, pheochromocytoma, somatostatinoma, and

vipoma

Laxative abuse (stimulant laxatives)

Medication and toxins

Mimics of Diarrhea

Pseudodiarrhea, or the frequent passage of small volumes of stool, is often associated with rectal

urgency, tenesmus, or a feeling of incomplete evacuation, and accompanies IBS or proctitis.

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