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DR.ANAM NAVEED KHAN

RESIDENT MEDICAL UNIT 4

CHK

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Name: Ayesha d/o Ateeq khan

Age: 20 yrs

Residence: Hyderabad

Status: Unmarried

D.O.A: 2-6-2011

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She presented with 1 month history of.

Swelling over both feet

Vomiting, loose motions

Abdominal pain

Severe weight loss

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1 month ago, the patient noticed swelling

over both limbs, initially mild but gradually it

progressed uptil thigh.

This was followed by vomitings, 4-6/day,

watery, non foul smelling, non bloody,

associated with nausea, anorexia, increased

thirst & central abdominal pain and withloose motions.

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Loose motions were watery, 6-8/day,

moderate in amount, non bloody, no mucus

present, but tenesmus and fecal

incontinence was present.

Patient also complains of dry skin,

generalized weakness, severe weight loss and

bone pains.

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Nothing significant.

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Appetite: decreased

Diet: normal

Sleep: normal

Micturation: no complains

Bowel habits: As per presenting complains

Addiction: nil

Weight loss: significant loss noticed

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K: 13 yrs

Flow: decreased during last cycle

Cycle: 4/30

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No history of TB in family, parents and

siblings alive and healthy.

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Belongs to a poor family.

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ABDOMEN: Pain in whole abdomen.

CHEST: No chest pain, cough, breathlessness etc.

CVS: No chest pain, dyspnea, PND, orthopnea orpalpitations.

CNS: No dizziness, blackouts, limb weakness etc.

MUSCULOSKELETAL: Generalizaed weakness, bonepains.

GENITO-URINARY: No complains.

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APPEARANCE:

Young girl of good height, cachectic,

pale, looking ill, lying on bed, conscious and

oriented x 3 and co-operative.

VITALS: B.P: 100/80 mm Hg

Pulse: 92b/min

R/R: 20/min

Temp: Afebrile

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Anemia ++

Dehydration ++

Edema ++

Tongue dry and smooth

Angular chelosis, dry skin

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INSPECTION:

Scaphoid shaped abdomen, centrally placedumbilicus, moving equally with respiration.Scratch marks all over abdomen.

PALPATION:

No tenderness, no visceromegaly, nolymphadenopathy. Free fluid present in flanks.

Shifting dullness positive.

AUSCULTATION:

Gut sounds normal.

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CHEST:

NVB all over chest with no addedsounds.

CVS:

S1+S2 audible in all 4 areas with noadded sounds.

CNS:

Grossly intact but generalized reducedmuscle bulk.

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20 yrs old Ayesha with no known comorbids

presented with 1 month history of bilateral

lower limbs swelling, vomiting & loose

motions, abdominal pain & severe weightloss. On general examinaion, she was vitally

stable, cachectic, moderately anemic &

dehydrated. Pedal edema & signs of vitamin

deficiency were present. Systemicexamination was significant for free fluid in

the abdomen.

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CBC:

Hb = 10.1 gm%

MCV = 96.2

MCH = 32.2TLC = 8.6

N = 72%

PLTs = 140,000

ESR:

10 mm in 1st hr

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UCE:

Na+ = 140meq/l

K+ = 3.1 meq/l

cl- = 107meq/l

BUN =3Creatinine + 0.5

RBS:

86mg%

LFTs =

T.bili = 0.83

SGPT = 23

Alk. phosohatase = 74

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Vitamin B12=

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PROTIEN A/G RATIO:

Total= 4.9

Albumin= 2.5

Globulin= 2.4Ratio= 1.0

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CALCIUM:

6.5 (corrected Ca= 7.7)

Mg=1.2 ( 1.6-2.6)

PHOSPHATE=

3.0 (2.7-4.5)

PT/INR:

1.44

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URINE D/R:

Sp.gravity = 1.01

Nitrites= +ve

Red cells= NilPus cells= 1-2

Casts= Nil

Bacteria= ++

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VIRAL MARKERS:

Hep B and Hep C negative by ICT.

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Normal

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ULTRASOUND ABDOMEN:

Increased echogenicity of liver, moderate

ascites.

MT:

Negative with 0 mm.

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ASCITIC D/R:

Appearance= turbid, blood stained

Proteins= 1gm%Albumin= 0.8gm%

Amylase= 12U/l

RBC= +++WBC= 57/mm3 (lymphos: 81%)

No organism seen----- AFB not seen

SAAG Ratio : 1.7

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CT SCAN ABDOMEN WITH CONTRAST:

Normal

MP:

Not seen

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OGD:

Gastritis, lax esophageal sphincter

Biopsies taken from antrum and D2.

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STOOL D/R:

ph= acidic

mucus= NilRBC= Nil

WBC= +/HPF

Parasite cyst/ ova= None

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SPUTUM AFBx 3:

Negative

TTG=

IgA: 4.57 (

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CBC repeated. Hb: 8.1

MCV: 101

TLC: 18.7Plts: 71,000

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Report of blood c/s showed staph aureus

(? Contamination).

Report of urine c/s showed no growth.

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COLONOSCOPY:

Normal GI mucosa. Biopsies taken from

sigmoid and caecum.

Retic count:

1.8%

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BIOPSY FROM ANTRUM AND D2:

Moderate chronic non specific duodenitis.

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BIOPSY REPORT OF SIGMOID AND CAECUM:

Mild to moderate non specific colitis.

ESR:

71 mm 1st hr

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HYDROGEN BREATH TEST:

Negative at 120 minutes

NOTE: In malabsorption, breath hydrogen

peaks (>20 ppm) at 60-90 min after lactose

ingestion.

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BARIUM STUDIES:

Due.

TSH:

Awaited

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MALABSORPTION SYNDROME

TYPE???????

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Defective absorption of fats, fat-soluble and other

vitamins, proteins, carbohydrates, electrolytes, minerals

and water.

Most common clinical presentation is chronic diarrhea.

Hallmark: Steatorrhea that causes excessive fecal fat

excretion and produces nutritional deficiencies and GIsymptoms.

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1. INTRALUMINAL DIGESTION

2. TERMINAL DIGESTIONIn the brush border of the small intestinal mucosa

3. TRANSEPITHELIAL TRANSPORT

Through vessels and lymphatic channels.

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Mechanism Specific Disease

Maldigestion Chronic pancreatitis, cysticfibrosis, pancreatic carcinoma

Bile Salt deficiency Cirrhosis, cholestasis, bacterialovergrowth, impaired ilealreabsorption, bile salt binders

Inadequate Absorptive surface Massive intestinal resection,

gastrocolic fistula, jejunoilealbypass

Lymphatic obstruction Lymphoma, Whipples disease,intestinal lymphangiectasia

Vascular disease Constrictive pericarditis, right-

sided heart failure, mesentericarterial or venous insufficiency

Mucosal disease Infection (esp.Giardia, Whipplesdisease, tropical sprue),Inflammatory diseases , radiation

enteritis.

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ABDOMINAL TUBERCULOSIS

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Tuberculous abdomen is a condition in which there

is tuberculous infection of the peritoneum or other

organs in the abdomen.

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Abdominal TB is usually secondary to

pulmonary TB.

Radiologic evaluation often shows noevidence of lung disease.

Active pulmonary disease is present in

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Nonhealing ulcers of the mouth or anus.

Difficulty swallowing with esophageal disease.

Abdominal pain mimicking peptic ulcer diseasewith stomach or duodenal infection.

Malabsorption with infection of the small

intestine.

Abdominal pain, diarrhea, or hematochezia withinfection of the colon.

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Is the most common area of involvement

Basis of which is the abundance of lymphoidtissue and slower rate of passage of luminal

contents.

However any area of GIT can be involved.

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Natural course of gastrointestinal tuberculosis maybe:

Ulcerative

Hypertrophic

Ulcero-hypertrophic

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1. Small intestines: Ulcerative form

2. Ileocaecal Region: Hypertrophic form

3. Tuberculous Mesenteric Adenitis

4. Tuberculous Peritonitis

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The cecum becomes conical, shrunken, and

retracted out of the iliac fossa due to fibrosis

within the mesocolon.

Ileocecal valve becomes fixed, irregular,

gaping, and incompetent.

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Acute tuberculous peritonitis

Chronic tuberculous peritonitis

Tuberculous stricture of the small

intestine causing subacute intestinal

obstruction

Ileo caecal tuberculosis presenting with a

mass in the right iliac fossa

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1. Ascitic Form

2. Encysted Form

3. Purulent Form

4. Dry Plastic Adhesive Form

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Abdominal Pain 90%

Fever 60%

Loss of Weight 60% Ascites 60%

Night Sweats 37%

Abdominal Mass 26%

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Abdominal TB mimics any abdominal

pathology, including cancers.

Skin tests are suggestive, but PPD testingcan be negative especially in patients

with weight loss or AIDS.

AFB stain and culture yield is very low.

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ULTRASONOGRAPHY

CT Scan

ENDOSCOPY, COLONOSCOPY:

May demonstrate mucosalhyperemia, an ulcerated mass, multiple

ulcers with steep edges and small sessilepolyps, small ulcers or erosions ordivertivcula most commonly in theileocecal region.

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Gastrointest Endosc 2004;59:362-8.

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Can show mucosal ulceration, thickening or stricture formation.

In the early stages, spasm and hypermotility with edema of theileocecal valve.

Later thickening of the ileocecal valve.

A widely gaping ileocecal valve with narrowing of the terminalileum (Fleischner sign)

A narrowed terminal ileum with rapid emptying of the diseasedsegment through a gaping ileocecal valve into a shortened, rigid,obliterated cecum (Stierlin sign)

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LAPAROSCOPY: Fluid for staining andculture and tissue for biopsy can beobtained.

Final diagnosis by either endoscopic orsurgical biopsy.

Biopsy reveals acid fast bacilli, caseatinggranuloma or positive cultures.

Detection of tubercle bacilli in biopsyspecimen by PCR is the most sensitivemeans of diagnosis.

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Intestinal obstruction

Fistula formation

Hemorrhage

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Once diagnosed, ATT is started.

1. Isoniazid

2. Rifampicin3. Pyrazinamide

4. Ethambutol

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Diagnostic Laparoscopy or Laparotomy

Therapeutic for:

Relieving obstructions

Removing Masses

Draining Abscesses

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Very good, if diagnosed before complications.

Complications increase morbidity and mortality.

Disseminated miliary TB has worse prognosis

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The definitive diagnosis of intestinaltuberculosis is made by:

Identification of the organism in tissue, either by

direct visualization with an acid-fast stain.

By culture of the excised tissue.

By a PCR assay.

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Can be established in:

A patient with active pulmonary TB and

radiologic and clinical findings that suggest

intestinal involvement.

Response to anti-TB therapy.

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CELIAC DISEASE

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Autoimmune disorder, prevalence of 0.5 to 1 percent in

the US.

HLA-DQ2 or HLA-DQ8.

Inappropriate immune response to the dietary proteingluten, which is found in rye, wheat, and barley.

Manifestations from no symptoms to overt

malabsorption with involvement of multiple organsystems.

Increased risk of some malignancies.

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PREVALENCE AMONG

RISK FACTOR THOSE WITH RISK FACTOR

Dermatitis herpetiformis 100%

1st degree relative with 5 to 22%

celiac disease

Autoimmune thyroid disease 1.5 to 14%

Down syndrome 5 to 12%

Turner's syndrome 2 to 10%

Type 1 diabetic:

Children 3 to 8%

Adults 2 to 5%

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Common

Diarrhea

Fatigue Borborygmi

Abdominal pain

Weight loss

Abdominal distention Flatulence

Uncommon

Osteopenia/ osteoporosis

Abnormal LFTs Vomiting

Iron-deficiency anemia

Neurologic dysfunction

Constipation Nausea

Up to 38 % Asymptomatic

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Serum IgA endomysial Ab and IgA tissuetransglutaminase Ab ( Sensitivity andspecificity > 95%)

Testing for gliadin antibodies is no longerrecommended because of the low sensitivityand specificity.

The tTG antibody is the recommended singleserologic test for celiac disease screening inthe primary care setting.

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Required to confirm the diagnosis of celiac

disease.

Should also be considered in patients withnegative serologic test results who are at high

risk.

Partial to total villous atrophy, or subtle cryptlengthening or increased epithelial

lymphocytes.

To avoid false-negative results, obtaining atleast four tissue samples is recommended.

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Normal small intestine

Celiac Disease Villous atrophy

Normal villi

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Gluten free diet.

Eliminate all wheat, rye, barley and their

derivatives.

May take 6-12 months for intestines to heal.

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Barley

Barley malt/extract

Bran

Couscous

Bromated or durum flour

Enriched or Self RisingFlour

Gram Flour

Flour/meal

Phosphated Flour

Rye

Semolina

Triticale (cross between

wheat/rye)

Wheat

Wheat Bran Wheat germ

Wheat starch

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Osteoporosis

Thyroid dysfunction

Deficiencies in folic acid, vitamin B12, fat-soluble vitamins, and iron

Increased risk of malignancy:

Non-Hodgkin's lymphoma (3-6x more likely)

Oropharyngeal, esophageal, and small intestinaladenocarcinoma.

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Protozoal infection of upper small intestine.

Caused by flagellate Giardia lamblia.

Most abundant in areas with poor sanitation.

Only the cyst form is infectious, trophozoites aredestroyed by gastric acidity.

Hypo-gammaglobulinemia, low IgA levels in gut,achlorydria, malnutrition are the favouringfactors.

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50% , no discernable infection.

10% , asymptomatic cyst passers.

25-50% , acute diarrheal illness------ followed bychronic diarrhea.

Abdominal cramps, bloating, flatulence, nausea,malaise & anorexia.

Stools greasy & frothy with no pus, blood or mucus.

Weight loss is common.

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Identification of cyst or trophozoites in stool.

Antigen assays.

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Metronidazole

Tinidazole

Nitazoxanide Furazolidine

Albendazole