30yr /f has c/o vomiting after eating and pain in lower abdomen usg shows minimal pod , mild wall thickning of small bowel with entritis with most likely subacute intestinal obstruction pt had constipation since 2 days

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Clinical Assessment: 30F with Subacute Small Bowel Obstruction + Enteritis + Minimal POD Fluid

Summary of Findings

Finding	Clinical Significance
Vomiting after eating	Suggests mechanical obstruction proximal GI tract
Lower abdominal pain	Consistent with small bowel / pelvic involvement
2 days constipation	Cardinal feature of partial/subacute obstruction
Mild small bowel wall thickening + enteritis on USG	Active inflammation/infection contributing to obstruction
Minimal free fluid in Pouch of Douglas (POD)	Reactive pelvic peritoneal fluid - low-grade peritonism or pelvic inflammatory process
USG impression: subacute intestinal obstruction	Partial/incomplete obstruction - more favorable prognosis

Understanding the Diagnosis

Subacute (Partial) Intestinal Obstruction is an incomplete obstruction where some bowel contents still pass. As stated in Bailey and Love's Surgery: "Incomplete obstruction is also referred to as partial or subacute." The classic quartet for complete obstruction (pain, distension, vomiting, absolute constipation) is only partially present here - she has relative constipation (2 days), not absolute constipation, which supports the subacute/partial picture.

Concurrent Enteritis (wall thickening on USG) suggests an inflammatory or infective etiology driving or complicating the obstruction. In a 30-year-old woman, important differential causes include:

Tuberculous enteritis with stricture (common in South Asia - subacute onset, wall thickening, partial obstruction)
Crohn's disease (transmural inflammation + stricture)
Infectious enteritis (bacterial - Salmonella, Yersinia; or parasitic) causing ileus/functional obstruction
Adhesions from prior surgery or PID (though no surgical history mentioned)
Pelvic Inflammatory Disease (PID) with secondary ileus - the minimal POD fluid + pelvic pain in a young woman makes this a key differential
Mesenteric adenitis causing functional obstruction
Intussusception (less common at 30 years; look for lead point)

Minimal POD (Pouch of Douglas) Fluid in a 30F is clinically significant - it indicates free fluid in the pelvic peritoneum. Causes to consider alongside obstruction:

Reactive to adjacent inflammation (enteritis/peritonism)
PID / tubo-ovarian pathology
Ruptured ovarian cyst (though typically more fluid)
Early peritonitis from bowel involvement

Immediate Management

1. Resuscitation (First Priority)

IV access - establish 2 large-bore IVs
IV fluid resuscitation - normal saline or Ringer's lactate
Correct electrolyte imbalances (vomiting causes hypokalemia, hypochloremia, metabolic alkalosis - check K+, Cl-, Na+, HCO3-)
NPO (nil by mouth) - bowel rest

2. Decompression

Nasogastric tube (NGT) insertion - decompresses stomach, reduces aspiration risk, reduces further bowel distension from swallowed air. Per Sabiston's Surgery: "Nasogastric decompression in a patient with small bowel obstruction has long been the standard of care."

3. Monitoring

Strict input/output charting including urine output (target >0.5 mL/kg/hr)
Vital signs every 4 hours - watch for fever, tachycardia (strangulation warning signs)
Serial abdominal examinations

4. Investigations to Order

Urgent bloods:

CBC (leukocytosis suggests strangulation or active infection)
CRP, ESR
LFT, RFT, electrolytes
Blood glucose
Serum lactate (if strangulation suspected)
Blood culture (if febrile)
Pregnancy test (beta-hCG) - mandatory in a 30F before any imaging/intervention

Imaging:

X-ray abdomen (erect + supine) - air-fluid levels, dilated bowel loops, no gas in rectum = complete obstruction; gas present = partial
CT abdomen + pelvis with contrast - gold standard to: (a) confirm obstruction, (b) identify transition point, (c) assess wall enhancement/ischemia, (d) evaluate pelvic organs, (e) identify enteritis/lymphadenopathy
Gynaecological review - pelvic USG already done; formal OBG consultation for POD fluid + lower abdominal pain in young woman

Other:

Stool routine + culture (if diarrhea component)
Mantoux / IGRA test (if TB suspected based on epidemiology)

5. Medications

Analgesia - IV paracetamol or titrated opiates (withhold NSAIDs given GI inflammation)
Antiemetics - IV ondansetron or metoclopramide
Antispasmodics - IV hyoscine/buscopan for colic
Antibiotics - if enteritis with infective cause suspected or signs of systemic infection: IV co-amoxiclav or piperacillin-tazobactam; cover for anaerobes if peritonism present
Antacids/PPI - IV pantoprazole/omeprazole

6. Conservative Trial vs. Surgery

Per Sabiston's Surgery: "Patients with a partial intestinal obstruction may be treated conservatively with resuscitation and tube decompression alone. Resolution of symptoms and discharge without the need for surgery have been reported in up to 85% of patients with a partial obstruction."

Continue conservative management if:

Symptoms improving (pain reducing, passing flatus, bowel sounds returning)
No fever, no tachycardia, no peritoneal signs
No leukocytosis or rising lactate
Repeat imaging shows no worsening dilation

Escalate to surgery if any of the following appear:

Signs of strangulation (fever, tachycardia, peritonism, leukocytosis, rising lactate)
Perforation (peritonitis, free air on X-ray/CT)
Clinical deterioration after 24-48 hours of conservative management
Complete obstruction on serial imaging

Special Considerations for This Patient (30F)

Gynaecological cause must be excluded: In a young woman with lower abdominal pain + POD fluid, always rule out PID, ectopic pregnancy, ovarian torsion, endometriosis. These can cause secondary ileus mimicking obstruction.
Pregnancy must be excluded before CT scan (radiation).
If PID is the driving cause: IV antibiotics (cefoxitin + doxycycline, or metronidazole + azithromycin) will be primary treatment; obstruction will resolve secondarily.
TB enteritis if clinically suspected (chronic symptoms, constitutional features, epidemiology): add anti-TB therapy after confirmation.

Red Flag Signs Requiring Immediate Surgical Review

Sudden worsening of abdominal pain (colicky becoming constant = strangulation)
Rebound tenderness / board-like rigidity
High fever > 38.5°C + leukocytosis > 15,000
Hemodynamic instability
Absent bowel sounds with progressive distension

References: Bailey and Love's Short Practice of Surgery (28th ed.), Sabiston Textbook of Surgery; Sleisenger & Fordtran's Gastrointestinal and Liver Disease.

Create a comparison table of differential diagnoses for subacute SBO in young women

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I have enough from the library plus my own clinical knowledge to build a thorough, well-referenced comparison table. Here it is:

Differential Diagnoses for Subacute Small Bowel Obstruction in Young Women

Comparison Table

Feature	TB Enteritis	Crohn's Disease	PID / Adnexal Pathology	Post-surgical / Adhesions	Endometriosis	Infectious Enteritis	Intussusception
Age group	Any; 20-40 common	15-35 (bimodal)	Reproductive age	Any (post-op)	20-40	Any	Adults: 20-40
Onset	Insidious/subacute	Subacute/chronic	Acute to subacute	Acute/subacute	Cyclic/subacute	Acute	Subacute/acute
Abdominal pain	RIF / periumbilical, colicky	RIF / periumbilical, colicky	Lower abdominal, bilateral	Central/diffuse, colicky	Cyclical, lower abdominal	Diffuse, crampy	Episodic colicky
Vomiting	Present (postprandial)	Present	Variable	Present	Variable	Present + diarrhea	Present
Constipation	Yes (partial)	Yes, alternates with diarrhea	No (or mild)	Yes	Yes, cyclical	No - usually diarrhea	Yes
Fever	Low-grade, evening rise	Low-grade	High-grade (>38.5°C)	Variable	Absent	Present, variable	Absent/mild
Menstrual link	None	None	Yes (dysmenorrhea, PID after menstruation)	None	Yes - cyclical pain	None	None
Vaginal discharge	Absent	Absent	Yes - purulent/mucopurulent	Absent	Absent	Absent	Absent
Constitutional symptoms	Weight loss, night sweats, anorexia	Weight loss, fatigue	Absent/mild	Absent	Absent	Absent	Absent
POD fluid on USG	Possible (ascites/lymph nodes)	Possible	Yes - common (pyosalpinx, tubo-ovarian abscess)	Rarely	Possible (endometrioma)	Possible (reactive)	Rare
Bowel wall thickening (USG/CT)	Yes - terminal ileum/ileocaecal	Yes - transmural, cobblestone	Mild reactive	Yes at adhesion site	Focal	Mild, diffuse	Yes (target sign)
Key USG/CT findings	Ileocaecal thickening, lymph nodes, ascites, omental caking	Skip lesions, creeping fat, fistula, mesenteric fat stranding	Thick-walled tubes, adnexal mass, pyosalpinx	Adhesive band, transition point, no wall thickening	Endometrioma ("chocolate cyst"), nodules on bowel	Diffuse wall thickening, free fluid	Target / donut sign
Lab findings	ESR/CRP elevated; Mantoux/IGRA +ve; ADA elevated	ESR/CRP elevated; fecal calprotectin elevated; anemia	WBC elevated; cervical swab +ve; STI screen	Mild leukocytosis	Normal or mild CRP	WBC elevated; stool culture +ve	Normal/mild leukocytosis
Prior history	TB contact, endemic area, immunosuppression, HIV	Family history IBD, prior flares	STI, multiple partners, IUCD, prior PID	Prior surgery (appendicectomy, C-section, gynaec surgery)	Dysmenorrhea, dyspareunia, infertility	Travel, contaminated food/water	None specific
Differentiating test	IGRA / Mantoux; colonoscopy + biopsy (granulomas); ascites ADA	Colonoscopy + biopsy (non-caseating granulomas); CTE/MRE	Cervical swab; TVUS; laparoscopy	CT with transition point; prior op records	MRI pelvis (gold standard); laparoscopy	Stool culture + PCR; blood culture	CT / USG (target sign); colonoscopy
First-line treatment	Anti-TB therapy (HRZE x 2 months, then HR x 4 months)	Steroids / 5-ASA / biologics; surgery for stricture	IV antibiotics (cefoxitin + doxycycline or ceftriaxone + metronidazole)	Conservative initially; adhesiolysis if fails	GnRH agonists / OCP; laparoscopic excision	Oral/IV rehydration; antibiotics if bacterial	Colonoscopic reduction; surgery if fails
Risk of strangulation	Low (unless complete)	Low-moderate	Low	Moderate-high (band adhesion)	Low	Low	Moderate (lead point)
Recurrence risk	Low (if treated)	High (relapsing-remitting)	Moderate if untreated	High (adhesion reformation)	High if not treated	Low	Low-moderate

Key Distinguishing Points for This Patient (30F, POD Fluid + Enteritis)

Clue	Points Toward
Lower abdominal pain + POD fluid	PID / adnexal pathology as primary cause
Bowel wall thickening + enteritis pattern	TB enteritis or Crohn's (both cause transmural inflammation)
Subacute onset + constipation 2 days	Partial mechanical obstruction from stricture (TB/Crohn) or adhesion
No fever documented	Less likely acute PID or infectious enteritis
Young woman in reproductive age	PID and endometriosis must be actively excluded
No surgical history mentioned	Adhesions less likely unless prior gynaec procedure (e.g., D&C, C-section)

Diagnostic Ladder for This Patient

Step 1: Exclude pregnancy (beta-hCG) and PID (cervical swab, WBC, TVUS)
Step 2: CT abdomen + pelvis with IV contrast → transition point? wall thickening? lymphadenopathy? adnexal mass?
Step 3: If ileocaecal thickening → IGRA / Mantoux + colonoscopy biopsy (TB vs Crohn)
Step 4: If pelvic/adnexal pathology → OBG consult + MRI pelvis
Step 5: If no other cause → consider adhesiolysis vs. diagnostic laparoscopy

References: Bailey and Love's Short Practice of Surgery (28th ed.); Sabiston Textbook of Surgery; Goldman-Cecil Medicine (22E); Fischer's Mastery of Surgery (8th ed.); Maingot's Abdominal Operations.

Surgery will be more effective

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small bowel obstruction conservative versus surgical management outcomes

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PMID: 28728984

This is a position that needs to be respectfully challenged based on current evidence. Here is a direct, evidence-based counter-argument:

Surgery is NOT the First-Line Choice for Subacute SBO - Here's Why

The Evidence Says the Opposite for This Patient

This patient has subacute (partial) intestinal obstruction - which is precisely the scenario where conservative management is the standard of care and surgery carries measurable risk without proportional benefit at this stage.

What the Data Shows

A 2017 meta-analysis by Hajibandeh et al. (PMID 28728984) pooling 876 patients comparing operative vs. non-operative management of SBO found:

Outcome	Operative	Conservative	Significance
Mortality	Higher (RD +0.03-0.04)	Lower	P = 0.01
Complications	5-8x higher (OR 5.39-8.14)	Lower	P < 0.00001
Recurrence	Lower	Higher	P = 0.0005
Hospital stay	No difference	No difference	P = 1.0
Re-intervention rate	No difference	No difference	P = 0.36

Conclusion from the meta-analysis: "The benefit of surgical treatment should be balanced with the risks associated with surgery. Surgical intervention could be preserved for cases with high suspicion or evidence of bowel strangulation."

Per Sabiston's Textbook of Surgery: "Resolution of symptoms and discharge without the need for surgery have been reported in up to 85% of patients with a partial obstruction."

Why Early Surgery in THIS Patient is Premature

Reason	Explanation
Partial/subacute obstruction	She is still passing some stool (2-day constipation, not absolute). Partial obstruction resolves conservatively in the majority.
No strangulation signs	No fever, no peritoneal signs described, no hemodynamic instability. Strangulation is the main indication that forces the surgical hand.
Underlying cause unknown	Operating without a diagnosis risks operating for the wrong thing. If this is TB enteritis, she needs anti-TB drugs - not surgery. If it's PID-related ileus, she needs antibiotics. Surgery on an inflamed, infected bowel in an underfed patient carries high anastomotic leak risk.
She is young (30F)	Surgery creates adhesions. Adhesions are themselves a leading cause of future SBO (the #1 cause in adults). You risk creating the very problem you are treating.
POD fluid present	Minimal free fluid + lower abdominal pain in a young woman mandates gynaecological exclusion before surgery. Operating and finding a gynaecological cause intraoperatively without proper preparation is avoidable with CT/OBG review first.

When Surgery BECOMES Necessary (Clear Indications)

Surgery is correct - but only when these are present:

Absolute Surgical Indications	Clinical Signs
Strangulation / ischemia	Fever + tachycardia + leukocytosis + constant (not colicky) pain + peritonism
Perforation	Board-like rigidity, free air on X-ray/CT
Complete obstruction not resolving	No improvement after 24-48h conservative trial; contrast not reaching colon at 24h
Closed-loop obstruction	CT evidence of volvulus or two-point fixation
Failure of conservative management	Worsening distension on serial imaging despite NGT + IVF
Clinical deterioration	Rising lactate, falling BP, worsening leukocytosis

The Right Sequence for This Patient

RIGHT NOW:
  NPO + IV fluids + NGT decompression + electrolyte correction
  → beta-hCG + CT abdomen/pelvis with contrast
  → OBG review for POD fluid
  → Blood cultures, CBC, CRP

AT 24-48 HOURS:
  Reassess:
    Improving? → Continue conservative, identify cause (scope/biopsy)
    Static?    → Water-soluble contrast challenge via NGT
    Worsening? → Surgical review, operate

OPERATE IF:
  Strangulation signs, perforation, or failed 48h conservative trial

Bottom Line

Early surgery for subacute/partial SBO increases mortality and complication rates by 5-8 fold without reducing hospital stay or re-intervention rates compared to a structured conservative trial. The evidence from both major surgical textbooks and the best available meta-analysis is consistent: operate on the complication, not on the obstruction itself - unless that obstruction is complete, failing to resolve, or showing signs of vascular compromise.

The goal right now is to stabilize, decompress, diagnose the cause, and reassess in 24-48 hours. Surgery remains available and should not be delayed if she deteriorates - but it is not the most effective first step for a patient with subacute, partial obstruction and no strangulation signs.

Crohns disease

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I now have comprehensive material from Robbins Pathology, Sabiston's Surgery, and Sleisenger & Fordtran to provide a thorough overview.

Crohn's Disease - Full Clinical Overview

1. Definition

Crohn's disease (CD) is a chronic, relapsing-remitting, transmural inflammatory bowel disease that can affect any part of the GI tract from mouth to anus, but most commonly involves the terminal ileum and proximal colon. Unlike ulcerative colitis, it is discontinuous, full-thickness, and associated with granuloma formation.

2. Epidemiology

Parameter	Detail
Incidence	3-20 per 100,000 / year (higher in Western countries)
Age of onset	Bimodal: 15-35 years (major peak) and 55-70 years (minor peak)
Sex	Slightly more common in females
Risk factors	Cigarette smoking (strong risk factor), first-degree relative with IBD, Jewish ethnicity, Westernized diet, appendicectomy
Geography	Higher in urban, developed nations; increasing in developing countries

3. Etiology and Pathogenesis

Crohn's disease results from an abnormal immune response in genetically susceptible individuals triggered by environmental factors and altered gut microbiome.

Factor	Role
Genetics	NOD2/CARD15 gene mutations (impaired bacterial recognition); >200 susceptibility loci identified
Immune dysregulation	Overactivation of Th1 and Th17 cells → excess TNF-α, IL-12, IL-23 → transmural inflammation
Gut microbiome	Decreased microbial diversity; reduced Firmicutes, increased adherent-invasive E. coli
Barrier dysfunction	Increased intestinal permeability in ~10% of first-degree relatives - a pre-disease marker
Environmental triggers	Smoking, NSAIDs, antibiotics, stress, dietary antigens

4. Pathology

Gross Pathology

Gross pathology of Crohn's disease: (A) Small intestinal stricture, (B) Linear ulcers creating cobblestone appearance with thickened wall, (C) Perforation and serositis, (D) Creeping fat (arrows) - Robbins Pathologic Basis of Disease

Gross Feature	Description
Skip lesions	Diseased segments separated by normal bowel ("skip areas") - pathognomonic
Cobblestone mucosa	Linear serpentine ulcers + edematous intervening mucosa
Transmural thickening	Rubbery, thickened bowel wall due to edema, fibrosis, muscle hypertrophy
Strictures	Fibrotic narrowing of lumen - leads to obstruction
Creeping fat	Mesenteric fat wraps around the bowel serosal surface
Fissures	Deep knife-like ulcers extending through the wall → abscess, fistula

Microscopic Pathology

Microscopic Feature	Detail
Transmural inflammation	Lymphoid aggregates throughout all layers of the bowel wall
Crypt abscesses	Neutrophils within crypts - sign of active disease
Non-caseating granulomas	Found in ~35% of cases; any layer of bowel wall or mesenteric lymph nodes - hallmark
Architectural distortion	Branching, disorganized crypts from repeated injury/repair cycles
Paneth cell metaplasia	In left colon (where normally absent)

Key point: Granulomas are non-caseating in Crohn's (vs. caseating in TB) - this distinction is critical in differentiating the two conditions in this patient.

5. Disease Distribution and Behaviour

Location (Montreal Classification)

Location	Frequency
Terminal ileum ± right colon (ileocaecal)	~40% - most common
Small bowel only	~30%
Colon only	~25%
Upper GI tract (mouth, oesophagus, stomach, duodenum)	~5%

Disease Behaviour (Montreal B Classification)

Type	Features
B1 - Inflammatory	Luminal inflammation without stricture/fistula; most common early pattern
B2 - Stricturing	Fibrotic narrowing → obstruction (this patient's likely pattern)
B3 - Penetrating	Fistulae, intra-abdominal abscesses
+ P modifier	Perianal disease (fistula, abscess, skin tags)

6. Clinical Features

Intestinal Features

Symptom	Detail
Abdominal pain	RIF / periumbilical, colicky; postprandial (obstructive pattern in stricturing disease)
Diarrhea	Non-bloody (small bowel CD) or bloody (colonic CD); typically chronic
Weight loss / anorexia	From malabsorption, protein loss, reduced intake
Vomiting	Postprandial; suggests obstruction at terminal ileum / stricture
Palpable RIF mass	Matted loops / mesenteric thickening / abscess
Fever	Low-grade (active disease) or high-grade (abscess, perforation)
Perianal disease	Fistulae, abscesses, skin tags, fissures - in >50% of cases

Per Robbins Pathology: "Approximately 20% present acutely with RLQ pain, fever, and bloody diarrhea mimicking appendicitis."

Extraintestinal Manifestations (EIMs)

System	Manifestation
Joints	Migratory polyarthritis, sacroiliitis, ankylosing spondylitis
Eyes	Uveitis, episcleritis
Skin	Erythema nodosum, pyoderma gangrenosum
Liver / Biliary	Pericholangitis, primary sclerosing cholangitis (less common than UC)
Other	Clubbing, renal oxalate stones (fat malabsorption), B12 deficiency (terminal ileal disease), iron deficiency anemia

EIMs may precede intestinal symptoms in some patients.

7. Diagnosis

Step 1 - Blood Tests

Test	Finding in Active CD
CBC	Leukocytosis, microcytic or macrocytic anemia
CRP / ESR	Elevated (correlates with disease activity)
Serum albumin	Low (protein-losing enteropathy)
Fecal calprotectin	Elevated - sensitive marker of intestinal inflammation; good correlation with relapse
ASCA (anti-Saccharomyces cerevisiae antibodies)	Positive in ~60-70% of CD; negative in UC
p-ANCA	Negative in CD (positive in ~75% of UC)
B12 / folate / iron / ferritin	Deficient in long-standing disease

Step 2 - Imaging

Modality	Findings
CT Enterography (CTE)	Mural thickening, mucosal hyperenhancement, mesenteric fat stranding, "comb sign" (engorged vasa recta), strictures, fistulae, abscesses
MR Enterography (MRE)	Gold standard for small bowel assessment; no radiation; preferred for young patients and follow-up
Ultrasound	Bowel wall thickening >4mm; loss of wall stratification; free fluid - useful in acute setting
Barium follow-through / small bowel series	String sign (tight terminal ileal stricture); cobblestone pattern; fistulae
Chest X-ray	Exclude TB (if relevant differential)

Step 3 - Endoscopy and Histology

Investigation	Findings
Colonoscopy + ileoscopy	Skip lesions, aphthous ulcers, cobblestoning, rectal sparing (50% of cases), pseudopolyps
Biopsy (multiple sites)	Non-caseating granulomas, crypt architectural distortion, transmural lymphoid aggregates
Upper GI endoscopy	If upper GI symptoms; aphthae in duodenum suggest CD
Capsule endoscopy	For suspected small bowel CD when CTE/MRE inconclusive (contraindicated if stricture present)

Crohn's vs. Ulcerative Colitis - Key Differences

Feature	Crohn's Disease	Ulcerative Colitis
Distribution	Any part of GI tract	Colon + rectum only
Pattern	Skip lesions	Continuous, from rectum upward
Rectal involvement	Spared in 50%	Almost always involved
Depth	Transmural	Mucosal only
Granulomas	Yes (35%)	No
Bleeding	Less common	Almost always
Perianal disease	Frequent (>50%)	Rare (<20%)
ASCA	Positive (~60%)	Negative
p-ANCA	Negative	Positive (~75%)
Fistulae	Common	Rare
Risk of cancer	Increased (colonic CD)	Significantly increased

8. Disease Activity Scoring

Crohn's Disease Activity Index (CDAI) - used in clinical trials and research:

Remission: CDAI < 150
Response to therapy: Decrease in CDAI ≥ 100 points
Severe disease: CDAI > 450

Note: CDAI uses 8 variables including stool frequency, abdominal pain, general wellbeing, extraintestinal manifestations, use of antidiarrheals, abdominal mass, hematocrit, and body weight.

9. Complications

Complication	Notes
Intestinal obstruction	Most common surgical complication; from fibrotic strictures (B2 disease)
Fistulae	Enteroenteral, enterocutaneous, enterovesical, rectovaginal
Intraabdominal abscess	From penetrating disease; percutaneous drainage preferred first-line
Free perforation	Rare but life-threatening
Malabsorption	B12 deficiency (terminal ileum), fat-soluble vitamins, iron, zinc
Oxalate renal stones	Fat malabsorption → increased oxalate absorption
Colorectal cancer	Risk increased in colonic CD; less than UC
Toxic megacolon	Rare (more common in UC)
Nutritional deficiencies	Protein-energy malnutrition, anemia

10. Treatment

Medical Management - Step-Up Approach

Mild CD                   → Aminosalicylates (mesalazine/sulfasalazine) - mainly colonic CD
                          → Antibiotics (metronidazole, ciprofloxacin) - perianal/fistulating
       ↓ Not responding
Moderate CD               → Oral/IV Corticosteroids (prednisolone 40mg/day) - induction only
                          → Budesonide (ileal-release) - for ileocaecal CD; less systemic side effects
       ↓ Steroid-dependent or steroid-refractory
Immunomodulators          → Azathioprine (AZA) / 6-mercaptopurine (6-MP) - maintenance
                          → Methotrexate (MTX) - if intolerant to AZA
       ↓ Still not controlled
Biologics                 → Anti-TNF: Infliximab (IV), Adalimumab (SC), Certolizumab (SC)
                          → Anti-integrin: Vedolizumab, Natalizumab
                          → Anti-IL-12/23: Ustekinumab
                          → JAK inhibitors: Upadacitinib (newer)
       ↓ Complications / Failure
Surgery

Drug Class	Drugs	Indication
Aminosalicylates	Mesalazine, sulfasalazine	Mild colonic CD; limited efficacy in small bowel
Corticosteroids	Prednisolone, budesonide, hydrocortisone IV	Induction of remission (NOT maintenance)
Immunomodulators	Azathioprine, 6-MP, methotrexate	Maintenance of remission; steroid-sparing
Anti-TNF biologics	Infliximab, adalimumab, certolizumab	Moderate-severe CD; fistulating disease
Anti-integrin	Vedolizumab, natalizumab	Biologic failure; gut-selective action
Anti-IL-12/23	Ustekinumab	Moderate-severe CD; fewer infections than anti-TNF
Antibiotics	Metronidazole, ciprofloxacin	Perianal disease, septic complications
Nutritional therapy	Elemental / polymeric feeds	Particularly in children; disease remission + nutrition

Key point: Corticosteroids are for induction only - never for maintenance. Mucosal healing (not just symptom relief) is now the therapeutic goal.

11. Surgical Management

Surgery does not cure Crohn's disease - recurrence at the anastomotic site is common (up to 40% within 10 years). Surgery is therefore reserved for complications.

Indications for Surgery

Indication	Procedure
Fibrotic stricture causing obstruction	Strictureplasty (bowel-preserving) or segmental resection
Failed medical therapy / intractable disease	Segmental resection
Fistulae not responding to medical therapy	Fistula excision ± bowel resection
Intraabdominal abscess	Percutaneous drainage (1st line); laparoscopic/open drainage if fails
Free perforation	Resection ± primary anastomosis / stoma
GI haemorrhage	Segmental resection
Cancer / dysplasia	Oncological resection
Perianal disease	Seton placement, fistulotomy, diversion ileostomy

Principles of Surgery in Crohn's

Bowel conservation is paramount - multiple resections lead to short bowel syndrome
Strictureplasty preferred over resection for short, fibrotic strictures
Minimal resection margins - 2cm macroscopic clearance is adequate (frozen section not required)
Laparoscopic approach preferred - lower morbidity, shorter stay
Preoperative optimization - stop biologics 4-8 weeks pre-op (increased infection risk); correct nutrition and anemia

12. Prognosis

Crohn's disease is lifelong - there is no cure
~80% of patients require surgery at some point in their lifetime
Recurrence at anastomosis in 40% within 10 years - necessitates bowel-sparing surgery
Smoking cessation is the single most important modifiable factor to reduce recurrence
The introduction of biologic therapies has significantly reduced surgery rates
Monitoring: regular colonoscopy from year 8-10 onwards (colonic CD) for dysplasia surveillance

References: Robbins & Cotran Pathologic Basis of Disease; Sabiston Textbook of Surgery (latest ed.); Sleisenger & Fordtran's Gastrointestinal and Liver Disease; Goldman-Cecil Medicine.

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