Diagnosis: A Symptom-based Approach in Internal Medicine CS Madgaonkar
INDEX
×
Chapter Notes

Save Clear


Abdominal DistensionCHAPTER 1

 
SYNOPSIS
Abdominal distension* may be defined as an increase in the girth of the abdomen. It is noticed by the patient because of the increase in belt or clothing size, recent weight gain, or ankle edema. Its onset may be sudden or gradual, persistent or intermittent. It may be entirely asymptomatic. More often the patient may describe distension as bloating,1,2 fullness, hardness, tightness or pressure. These symptoms are usually exacerbated by meals, fluctuate in intensity, and are worse in the day and settle overnight. Other symptoms such as belching, postprandial discomfort, nausea, vomiting, shortness of breath, localized pain, and constipation, if present, may provide clues for the etiology of abdominal distension. As a mnemonic device the causes can be remembered as five ‘fs’: fat (obesity), fluid (ascites), flatus (gastrointestinal), fetus (pregnancy), and feces (constipation). However, abdominal distension/bloating may be contributed to by several simultaneous conditions, and the diagnosis may be particularly challenging, especially in a subset of patients with functional GI disorders (FGIDs).36 A careful history and physical examination are necessary to develop an ade-quate differential and investigations, including psychosocial evaluation, that will help in the cost-effective approach to the diagnosis and care of these patients, who are otherwise susceptible to receiving unnecessary, costly, and sometimes risky studies and treatments.7
 
DIFFERENTIAL DIAGNOSIS
 
Common
  • FGIDs (vide infra ↓↓): (aerophagia; IBS, globus; rumination syndrome: vide infra↓↓; dysmotility-like dyspepsia; gallbladder dysfunction; proctalgia fugax:vide infra↓↓)
  • Infestations diarrhea (giardiasis)
  • Obesity (metabolic syndrome)2
  • Pregnancy
  • Distended bladder
  • Ascites
  • Intra-abdominal lump (organomegaly, tumor, cyst, neoplasm).
 
OCCASIONAL
  • Peritonitis (bacterial, tubercular, perforated viscus)
  • Intestinal obstruction (strangulated hernia, adhesions, fecal impaction)
  • Paralytic ileus (intra-abdominal inflammation, metabolic, drug induced).
 
RARE
  • Ascites (constrictive pericarditis, portal hypertension, Meigs syndrome: vide infra ↓↓).
  • Peritonitis (spontaneous bacterial peritonitis, i.e. SBP:vide infra↓↓, malignancy)
  • Toxic megacolon (pseudomembranous colitis, ulcerative colitis)
  • Pneumoperitoneum (traumatic rupture or perforation of viscus)
  • Malabsorption syndromes (secondary lactase deficiency)
  • Hypoalbuminemia (malnutrition, liver failure).
 
INVESTIGATIONS—GENERAL
 
CBC
  • Leukocytosis in bacterial infection, inflammation (e.g. infestations diarrhea, peritonitis); eosinophilia in parasitic infection
  • Microcytic or megaloblastic anemia in malabsorption syndrome.
 
ESR
  • Elevated in infection, inflammation and malignancy.
 
Urinalysis
  • Albuminuria in renal disorders
  • Urobilinogenuria may be present in hepatic disorders, absent in complete biliary obstruction
  • In women, hCG to rule out pregnancy.
 
Stools
  • Ova, cysts, and parasites; rule out giardiasis
  • Occult blood in carcinoma
  • Steatorrhea in malabsorption syndromes.
 
LFTs
  • Bilirubin (mostly conjugated) often elevated
  • Aminotransferases like ALT (i.e. SGPT), AST (i.e. SGOT) markedly elevated in cirrhosis of the liver
  • Alkaline phosphatase (ALP) elevated in any biliary obstruction.
 
AXR
  • Dilated loops of intestine with multiple air-fluid levels in intestinal obstruction.
 
US Abdomen/Pelvis
  • Can confirm the presence of ascites suspected at physical examination
  • Can detect as little as few milliliters of fluid located in obscure area, such as subdia-phragmatic region
  • Can help determine the cause of ascites such as cirrhosis, portal hypertension, portal and hepatic vein thrombosis
  • Can guide paracentesis; particularly useful in the presence of small amount of ascitic fluid or when the fluid is compartmentalized3
  • To assess organomegaly, hepatobiliary obstruction, and presence of a mass
  • In women—to evaluate pregnancy, uterine, or ovarian lesion.
 
INVESTIGATIONS—SPECIFIC
 
Tuberculin or PPD and Casino's Test
  • In TB and hydatid cyst.
 
Serum Lipase
  • May be elevated with pancreatic carcinoma, pancreatitis or perforated viscus.
 
CT/MRI Scan
  • Often has a complimentary role with US in the evaluation of patients with ascites, especially in patients with obscure source of ascites
  • Can evaluate and confirm intra-abdominal or retroperitoneal mass lesion
  • Valuable in the diagnosis of acute distension of abdomen suspected to be due to trauma, ruptured viscus, hemorrhage, obstruction, bowel ischemia, or leaking abdominal aneurysm.
 
MRI Angiography
  • In patients with hepatic or portal vein thrombosis or obstruction by tumor.
 
Diagnostic Paracentesis
  • Ascitic fluid analysis for Gram's stain, AFB, culture and cytology
  • Estimation of amylase, lipase, and trigly-cerides to rule out pancreatitis and chylous ascites
  • Recent statistical data indicate that the exudate-transudate concept should be discarded in the classification of ascites because the estimation of the serum ascites albumin gradient (SAAG: Table 1.1) and ascitic fluid cholesterol is found to be a better marker in the diagnosis of ascites due to:
    • Portal hypertension (a high gradient > 1.1 g/dl indicates that the ascites is due to portal hypertension; and a low gradient <1.1 g/dl indicates ascites of nonportal hypertensive etiology8,9
    • To distinguish malignant from non-malignant causes of ascites.10
Table 1.1   Causes of ascites by the serum ascites albumin gradient (SAAG)
High gradient (>1.1 g/dl)
• Cirrhosis*
• Alcoholic hepatitis
• Fulminant hepatic failure
• Massive liver metastasis
• Congestive cardiac failure, constrictive pericarditis (cardiac ascites)
• Myxoedema, Budd-Chiari syndrome (hepatic vein thrombosis), or Veno-occlusive disease.
Low gradient (<1.1 g/dl)
• Peritoneal tuberculosis
• Nephrotic syndrome
• Peritoneal carcinomatosis
• Pancreatic ascites
• Biliary ascites
• Bowel obstruction/infarction
* Patients with high SAAG most often have portal hypertension.
 
Laparoscopy with Biopsy
  • Direct visualization of abdominal and pelvic organs to detect extra-abdominal mass, peritoneal deposits of tumor, TB, or meta-static disease of the liver. Biopsies are taken under direct vision to enhance diagnostic accuracy.
 
Exploratory Laparotomy
  • In undetermined etiology with adequate investigations.4
 
CLINICAL NOTES
  • Acute abdominal distension may signal life-threatening peritonitis or acute intestinal obstruction. A rapid check for signs of hypovolemia, such as pallor, thready pulse, diaphoresis, hypotension, altered mentation and focussed physical examination is indicated for urgent diagnosis and management
  • While dealing with patients with FGIDs, developing an effective patient-physician relationship through empathy, reassurance, and education is most rewarding
  • History—Includes onset, duration; weight gain (BMI >30 kg/m2); weight loss (tubercular abdomen, diabetic gastroparesis, anorexia nervosa, malignancy); bowel movements—constipation, diarrhea or altered bowel habits (IBS, malignancy); diet (excess fiber, milk or its products); medications (diphenoxylate, cisapride); substance use or abuse (laxatives, ecstasy); personal/social stress factors (food habits, smoking, alcohol); and family history (diverticulosis, polyposis)
  • Physical examination—Febrile episodes; abdominal tenderness, dilated veins, bowel sounds or mass; inguinal and femoral hernia; measuring the abdominal girth for a baseline value; and pelvic examination in women are important
  • Physical tests for ascites such as flank dullness, shifting dullness, and the puddle sign are not helpful when a small volume (less than 1 liter) of ascites exists
  • Ascites is rarely the sole physical finding. Once identified, investigations should follow to determine its cause
  • Development of symptoms of fever, abdominal pain, or mental status changes (encephalopathy) in a patient with ascites indicates complication such as SBP which has poor prognosis
  • Mixed ascites, i.e. ascites from two different causes may coexist in few patients with ascites, e.g. cirrhosis of the liver with CHF/ pancreatitis/tuberculosis/malignancy.
 
RED FLAGS
  • Aerophagia is not always ‘neurotic’; swallowing air may be a response to abdominal discomfort from organic disease
  • Patients with FGIDs with psychological difficulties such as depression, panic, somatization, and personality disorders may need psychologist or psychiatric referral
  • Swallowed air (aerophagia) that is not eructed may get trapped in the splenic flexure (colon makes a 90 degree turn at this location) causing distension with gas of that part of the large intestine in the region of the spleen. Since this location is just beneath the diaphragm, the location of the pain appears to be coming from the lower left chest, causing discomfort or pain which may be referred to left side of chest, shoulder or arm. This splenic flexure syndrome (SFS) may be mistaken for a coronary event. However, it may be distinguished from cardiac pain by its intermittent, colicky behavior and fluctuations in intensity of the pain. Also relief of pain of SFS is characteristically obtained by defecation.
 
SELECTIVE GLOSSARY
 
Functional GI Disorders (FGIDs)7, 11, 12
FGIDs is defined as a variable combination of chronic or recurrent GI symptoms not explained by structural or biochemical abnormalities. It cannot be diagnosed through endoscopic, radiologic, or laboratory studies. Furthermore, even though these disorders share certain physiologic characteristics (such as abnormal 5motility and visceral hypersensitivity) that are associated with symptom generation, the findings are not specific for diagnosis, and the clinician has limited ability to evaluate them in practice. In the absence of any objective marker, the identification and classification of FGIDs are based on symptoms, and consist of a wide spectrum of syndromes which cross over and in some cases overlap various anatomic areas of the luminal gut. Although IBS has traditionally been the most studied and written about, FGIDs constitute a number of unique disorders, including functional esophageal disorders (noncardiac chest pain, functional dysphagia, and globus sensation); functional dyspepsia (pain, discomfort, nausea, and other symptoms above the navel in persons who do not meet the diagnostic criteria for IBS); functional abdominal pain syndrome; functional abdominal bloating; functional diarrhea; functional disorders of the biliary tract, including Oddi sphincter; functional disorders of the anorectal area, such as pelvic floor dyssynergia; and proctalgia fugax. The diagnosis of FGIDs relies heavily on the clinical history, a limited diagnostic evaluation and early symptomatic treatment that include symptom monitoring and reassessment. There is increasing evidence that psychopharmacologic and psycho-therapeutic management of FGIDs are highly effective and, in many instances, surpass the efficacy of standard medical treatment.
 
Meigs Syndrome
Meigs syndrome is defined as the triad of benign ovarian tumor with ascites and pleural effusion that resolves after resection of the tumor. The ovarian tumor in Meigs syndrome is a fibroma. Pseudo-Meigs syndrome consists of pleural effusion, ascites, and benign tumors of the ovary other than fibromas. Pseudo-pseudo Meigs syndrome includes patients with systemic lupus erythematosus and enlarged ovaries.
 
Proctalgia Fugax
Proctalgia fugax is a diagnosis of exclusion, and defined as sudden, severe pain in the anorectal region lasting several seconds or minutes, and then disappearing completely. It is common but largely underreported. The etiology is not well-defined. Attacks are infrequent, left-sided, and short-lived. Patients are asymptomatic between episodes. The discomfort is usually triggered by stressful event; can occur during the day or night; although it is not typically associated with bowel movements, it may be relieved by heat, anal dilatation, or relaxation techniques.
 
Rumination Syndrome
Rumination means repeated regurgitation (backflow of food from the stomach into the mouth) and rechewing of food, i.e. voluntary or involuntary regurgitation and rechewing of partially digested food that is either re swallowed or expelled. This regurgitation appears effortless, may be preceded by a belching sensation, and typically does not involve retching or nausea. In rumination, the regurgitant does not taste sour or bitter. The behavior must exist for at least 1 month, with evidence of normal functioning prior to onset. Rumination occurs within a few minutes postprandial and may last 1-2 hours. Though frequency may vary, rumination typically occurs daily and may persist for many months or years. Although the etiology of rumination is unknown, multiple theories have been advanced to explain the disorder. These theories range from psychosocial factors to organic origins. Cultural, socioeconomic, organic, and psychodynamic factors have been implicated.6
 
Spontaneous Bacterial Peritonitis (SBP)
SBP is a bacterial infection of ascitic fluid in patients with decompensated cirrhosis. The term ‘spontaneous’ distinguishes this from surgical peritonitis. Enteric organisms are isolated from more than 90% of infected ascites fluid in SBP, suggesting that the GI tract is the source of bacterial contamination. Symptoms of infection occur in most patients with SBP, including fever, abdominal pain, mental status changes, and ileus. A high index of suspicion should exist for SBP in patients with cirrhosis and ascites, especially in those who do not improve following administration of diuretic medication.
REFERENCES
  1. Lea Richard, et al. Expert Commentary-Bloating, Distension, and IBS. Medscape General Med. 2005; 7(1): 18. web site: http://www.med-scape.com/viewarticle/483079_print. Accessed on28-08-08.
  1. Agrawal A, et al. Review article: Abdominal bloating and distension in functional gastro-intestinal disorders-epidemiology and exploration of possible mechanisms. Aliment Pharmacol ther. 2008;27(1):2–10. Epub 2007 Oct 11. [PMID: 17931344: Abstract].
  1. Crowell MD. Future treatment approaches for Functional GI Disorders. http://www.gastro.org/user-assets/Documents/08_Publications/06_GIHep_Annual_Review/Articles/Crowell.pdf. Accessed on 27-08-08.
  1. Jiang X, et al. Prevalence and risk factors for abdominal bloating and visible distention: A population-based study Gut. 2008; 57(6):756–63. [PMID: 18477677: Free full text].
  1. Azpiroz F, et al. The pathogenesis of bloating and visible distension in irritable bowel syndrome. Gastroenterol Clin Nortn Am 2005; 34(2):257–69. [PMID: 15862934: Abstract].
  1. Azpiroz F, et al. Abdominal bloating. Gastro-enterology. 2005; 129(3):1060–78. [PMID:16143143: Abstract].
  1. Drossman DA. Diagnosing and Treating Patients with Refractory Functional Gastrointestinal Dis-orders. Ann Intern Med 1995; 688–97. [PMID: 7574225: Abstract].
  1. Runyon BA, et al. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med 1992; 117(3):215–20. [PMID: 1616215: Abstract].
  1. Wong CL, et al. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results? JAMA 2008; 299(10):1166–78. [PMID: 18334692: Abstract].
  1. Rana SV, et al. Usefulness of ascitic fluid cholesterol as a marker for malignant ascites. Med Sci Monit 2005; 11(3):CR136–42. [PMID: 15735567: Abstract].
  1. Coraazziari E, et al. Definition and epidemiology of functional gastrointestinal disorders. Best Pract Res Cli Gastroentrol 2004; 18(4):613–31. [PMID: 15324703: Abstract].
  1. Jones MP, et al. Functional Gastrointestinal Dis-orders: An Update for the Psychiatrist. Psycho-somatics 2007; 48:93–102 [PMID: 17329601: Free full text].