Sciatica

Definition

• Bailey and Love's Short Practice of Surgery, 28th Edition

Causes (Etiology)

• Herniated nucleus pulposus (most common)
• Spinal canal stenosis (central, lateral recess, or foraminal)
• Spondylolisthesis
• Synovial cyst (from facet joint degeneration)
• Arachnoid or perineural (Tarlov) cysts
• Tumor: neurofibroma, ependymoma, or metastatic disease (prostate, breast, myeloma)
• Infection: epidural abscess, discitis, herpes zoster, Lyme disease
• Inflammatory radiculopathy (sarcoidosis, paraneoplastic)

• Lumbosacral plexopathy
• Sciatic neuropathy (e.g., piriformis syndrome)
• Peripheral neuropathy

• Hip arthritis, trochanteric bursitis
• Sacroiliac joint disease
• Iliotibial band syndrome, hamstring tendinitis
• Peripheral vascular disease

• Catamenial sciatica - endometriosis involving the sciatic nerve at the sciatic notch (linked temporally to premenstruation)
• Piriformis syndrome - the sciatic nerve runs through or near the piriformis; hypertrophy/spasm can cause buttock pain and vague sciatic symptoms
• Goldman-Cecil Medicine, Table 369-5 | Adams and Victor's Principles of Neurology, 12th Ed.

Clinical Presentation

• Unilateral leg pain radiating into the buttock, posterolateral thigh, leg, foot, and/or toes
• Often accompanied by low back pain
• Pain worsened by movement, coughing, sneezing, Valsalva
• Pain relieved by rest or recumbency
• Straight leg raise (Lasègue sign): pain reproduced when the ipsilateral leg is raised while supine - a hallmark test

• Bradley and Daroff's Neurology in Clinical Practice

Imaging

Red Flags - Cauda Equina Syndrome (Emergency)

• Saddle anesthesia (perineal numbness)
• Urinary/fecal retention or incontinence
• Bilateral leg weakness
• Progressive neurological deficit

• Bailey and Love's Surgery, Table 37.1

Treatment

Conservative (First-line)

• Activity: Early mobilization is better than bed rest; prolonged immobilization is detrimental
• Analgesics: NSAIDs are the primary pharmacologic option (though less effective for radicular than non-specific back pain); limited opioids for severe pain
• Physical therapy: Back-strengthening exercises, avoidance of straining maneuvers
• Spinal manipulation: Small reduction in pain up to 12 weeks

• Muscle relaxants - insufficient evidence
• Antiepileptics (gabapentin - small study benefit; pregabalin - not helpful for acute or chronic sciatica per Goldman-Cecil)
• Antidepressants - not recommended
• Oral corticosteroids - no lasting measurable benefit
• Tintinalli's Emergency Medicine | Goldman-Cecil Medicine | Bradley and Daroff's Neurology

Epidural Steroid Injection

• No significant functional benefit
• Does not reduce need for surgery
• No proven longer-lasting value
• An option for moderately-to-severely symptomatic patients as follow-up (not an ED procedure)

Surgery

• Severe or progressive neurological deficits
• Failure of nonoperative therapy after 6 weeks
• Cauda equina syndrome (urgent/emergent)
• Spinal instability
• Neurological deficits critical to the patient's vocation

Prognosis

• 70% of acute sciatic episodes resolve within 3 months
• Workers off work >6 months with back pain have a guarded prognosis for return to work
• Physicians should emphasize exercise, avoid deconditioning, and enable early return to graded work for pain lasting >4 weeks

Typhoid Fever - Complete Overview with Pathophysiology Flowchart

Pathophysiology Flowchart

INGESTION OF S. Typhi / S. Paratyphi
(contaminated food or water, fecal-oral route)
          │
          ▼
GASTRIC ACID BARRIER
  ├─ Normal acid → most organisms killed
  └─ Achlorhydria / large inoculum → organisms survive
          │
          ▼
SMALL INTESTINE (Terminal Ileum)
S. Typhi penetrates intestinal epithelium via M cells
overlying Peyer's patches
          │
          ▼
UPTAKE BY MONONUCLEAR PHAGOCYTES
in the lamina propria (submucosal lymphoid tissue)
  • Unlike NTS: NO massive neutrophil infiltration
  • Mononuclear (macrophage) predominant response
  • Key virulence factor: Vi antigen (capsule) resists
    phagocytic killing → intracellular survival
          │
          ▼
PEYER'S PATCHES ENLARGE
Plateaulike elevations up to 8 cm in terminal ileum
          │
          ├──────────────────────────────────────────┐
          ▼                                          ▼
PRIMARY BACTEREMIA                        LYMPHATIC SPREAD
(1st-2nd week)                     Organisms travel to mesenteric
  • Organisms enter portal circulation     lymph nodes → reactive
  • Seeded into liver, spleen,             hyperplasia
    gallbladder, bone marrow              Bacteria-laden phagocytes
  • Blood cultures POSITIVE (90%)          accumulate
          │
          ▼
MULTIPLICATION INSIDE MACROPHAGES
(in liver, spleen, bone marrow, lymph nodes)
  • "Typhoid nodules" - small foci of parenchymal
    necrosis with macrophage aggregates in liver,
    bone marrow, lymph nodes
  • Spleen: red pulp expansion from phagocyte hyperplasia
  • Relative bradycardia (endotoxin effect on myocardium)
          │
          ▼
SECONDARY (SUSTAINED) BACTEREMIA
(end of Week 1 → Week 2–3)
  • Massive re-seeding from intracellular reservoir
  • Systemic cytokine release (IL-1, TNF, IL-6)
  • Sustained high fever (38.8–40.5°C) for weeks
  • Rose spots: small erythematous maculopapular
    lesions on trunk/chest (S. Typhi in punch biopsy)
          │
          ├────────────────────┬────────────────────┐
          ▼                   ▼                    ▼
    GALLBLADDER          INTESTINAL           SYSTEMIC ORGANS
    SEEDING             CHANGES              (Week 2–4)
  • Organisms survive    (Week 3–4)
    in bile, gallstones  Peyer's patch
  • Chronic carrier state  hyperplasia →
    (2–5%) → re-excrete   necrosis → ulceration
    via bile into gut     (oval ulcers along long
  • ↑ Risk of             axis of ileum)
    gallbladder cancer         │
                         ┌─────┴──────┐
                         ▼            ▼
                   PERFORATION    HEMORRHAGE
                   (~1%)          (~6%)
                   (life-          (life-
                   threatening)    threatening)
                   Peritonitis     Bowel resection
                         │
                         ▼
                   COMPLICATIONS (~27% of hospitalized)
                   • Neurologic: meningitis, Guillain-Barré,
                     encephalopathy ("muttering delirium",
                     "coma vigil"), neuritis
                   • Cardiac: myocarditis, endocarditis,
                     pericarditis
                   • Pulmonary: pneumonia
                   • Renal: glomerulonephritis, HUS
                   • Hematologic: DIC, hemophagocytic syndrome
                   • Hepatobiliary: hepatitis, splenic/hepatic
                     abscess, cholecystitis
                   • MSK: osteomyelitis, arthritis

Key Pathophysiologic Mechanisms Explained

Why S. Typhi is uniquely systemic (unlike other Salmonella)

• S. Typhi evolved as a systemic pathogen through gene loss - it cannot effectively colonize the intestinal tract but excels at intracellular survival inside macrophages.
• The Vi capsular antigen resists complement-mediated killing and inhibits opsonization, enabling survival inside phagocytes.
• NTS causes neutrophil-driven diarrhea via IL-8; S. Typhi causes mononuclear infiltration and silent mucosal invasion without early diarrhea.
• Harrison's Principles of Internal Medicine, 22nd Ed.

Peyer's Patch Pathology (the histological hallmark)

• S. Typhi enters via M cells overlying Peyer's patches → taken up by submucosal mononuclear cells → patches enlarge into raised plaques (up to 8 cm) → necrosis → mucosal shedding → oval ulcers oriented along the long axis of the ileum.
• This is why perforation and hemorrhage occur in Weeks 3-4 at the ileocecal region - this is where Peyer's patches are densest.
• Robbins' Basic Pathology | Robbins' Pathologic Basis of Disease

Typhoid Nodules

• Liver
• Bone marrow
• Lymph nodes

Chronic Carrier State

• 2-5% become chronic carriers (shedding >1 year in stool or urine)
• S. Typhi survives in the gallbladder by forming biofilms on gallstones and invading gallbladder epithelial cells
• Chronic carriage is associated with increased risk of gallbladder cancer
• More common in women, infants, those with biliary abnormalities, or concurrent Schistosoma haematobium bladder infection

Clinical Course Timeline

Organism & Transmission Summary