Penile Fracture

Definition and Anatomy

Epidemiology and Mechanism

• Most commonly caused by excessive, sudden angulation of the erect penis against the perineum or partner's perineum during vigorous vaginal intercourse
• Also reported with masturbation, rolling over onto an erect penis, or forceful bending
• The laceration is classically found on the pendulous/distal shaft, though more proximal tears occur
• There is frequently a delay in presentation due to patient embarrassment

Clinical Features

Classic Presentation - the "3 P's":

1. Pop/crack - audible snapping sound as the tunica tears
2. Pain - immediate sharp pain
3. Penile swelling + rapid detumescence - the erection instantly deflates

Physical Examination

• "Eggplant deformity" (also called "aubergine penis"): swollen, ecchymotic, dark-colored penile shaft from expanding hematoma
• Deviation of the penis away from the side of the tear (the "rolling sign")
• The fracture line may be palpable as a defect in the tunica
• A clot often overlies the cavernosal rupture site
• If Buck's fascia (the deep fascia) is intact, hematoma stays confined to the penile shaft; if it ruptures, bruising spreads to the scrotum, perineum, or lower abdomen in a "butterfly" distribution

Associated Urethral Injury

• Occurs in approximately 20% of cases
• Suggested by: hematuria, inability to void, blood at the urethral meatus
• Requires retrograde urethrography (RUG) to rule out

Diagnosis

Management

Surgical (Standard of Care)

1. Deglove penis via circumcising subcoronal incision OR penoscrotal incision
2. Evacuate hematoma
3. Identify and inspect the full length of both corpora and urethra
4. Close corporeal laceration with absorbable sutures (e.g., 2-0 or 3-0 PDS or Vicryl) in interrupted or running fashion
5. If urethral injury present: repair over a catheter
6. Skin closure

Non-operative Management

• High rates of penile curvature (Peyronie's disease)
• Abscess formation
• Erectile dysfunction
• Prolonged recovery
• This approach is not recommended by any major guideline.

Outcomes

• Low complication rates
• Good erectile function preservation
• Avoidance of disabling penile curvature

Complications

Key Points Summary

• Fracture of the tunica albuginea of the erect penis
• Classic triad: pop + pain + rapid detumescence with "eggplant deformity"
• 20% have associated urethral injury - always evaluate
• Diagnosis is clinical; imaging (US, MRI) reserved for equivocal cases
• Immediate surgical repair is the treatment of choice
• Non-operative management should not be performed

Irritable Bowel Syndrome (IBS)

Definition

Epidemiology

• Worldwide prevalence: 4.1% (Rome IV criteria); higher with older Rome III criteria (~9%)
• More common in women (5.2%) than men (2.9%)
• Estimated incidence: ~38 per 10,000 person-years
• Up to 50% of affected individuals never seek care, yet IBS generates ~4.4 million physician visits/year in the US
• Associated with significant healthcare costs, absenteeism, and impaired work productivity
• Patients are more likely to undergo unnecessary diagnostic tests and surgeries

Subtypes (Rome IV)

Pathophysiology

1. Visceral Hypersensitivity

• The primary and most consistent finding
• Lowered pain thresholds to intestinal distention (allodynia/hyperalgesia)
• Mediated through sensitized afferent neurons and altered CNS processing

2. Altered Motility

• Colonic transit is generally slower in IBS-C and faster in IBS-D
• No single motility pattern is specific to IBS
• Exaggerated responses to meals, CCK, and mechanical stimuli are reported

3. Gut Microbiota (Dysbiosis)

• Colonization of germ-free animals with IBS microbiota induces visceral hypersensitivity, impairs intestinal permeability, and alters GI transit
• Gram-negative dysbiosis downregulates the serotonin reuptake transporter (SERT) in the mucosa

4. Abnormal Serotonin Pathways

• Serotonin-containing enterochromaffin cells are increased in IBS-D
• Postprandial serotonin levels are elevated in IBS-D patients
• TPH1 (tryptophan hydroxylase 1) polymorphisms are associated with IBS subtypes

5. Mucosal Immune Activation

• Low-grade mucosal inflammation with mast cell activation
• Increased cytokines/chemokines may explain extra-GI symptoms (fatigue, myalgia, anxiety)

6. Increased Intestinal Permeability

• "Leaky gut" allows antigen exposure to immune cells in the lamina propria

7. Altered CNS Modulation

• Abnormal central processing of visceral pain signals
• Strong association with psychosocial factors (anxiety, depression, trauma)

8. Bile Acids

• Up to 25% of IBS-D patients have idiopathic bile acid diarrhea
• Reduced FGF-19 synthesis by the ileal mucosa impairs negative feedback on bile acid synthesis
• Excess colonic bile acids accelerate transit, increase permeability, and cause visceral hypersensitivity

Risk Factors

• Genetic predisposition (familial clustering; 1.75-2.75x increased risk in relatives)
• Adverse childhood experiences
• Post-infectious IBS (after acute gastroenteritis - well established)
• Food triggers
• Psychological stress

Diagnostic Criteria

Rome IV Criteria (2016) - Current Standard

1. Related to defecation
2. Associated with a change in frequency of stool
3. Associated with a change in form (appearance) of stool

• Abnormal stool frequency (<3/week or >3/day)
• Abnormal stool form (hard/lumpy or loose/watery)
• Defecation straining, urgency, or incomplete evacuation
• Passing mucus

Clinical Features

GI Symptoms

• Crampy, lower abdominal pain - often postprandial
• Pain attacks: median 5.4/month, median duration 2.8 hours
• Bloating and abdominal distension (more prominent in IBS-C)
• Altered bowel habits - diarrhea, constipation, or both
• Mucus in stool
• Sensation of incomplete evacuation

Extra-GI Symptoms (very common)

Features Supporting IBS

• Recurrence over time without progression
• Onset during periods of stress
• Absence of fever, weight loss, bleeding
• Small-volume stools without blood
• Symptoms improve (or worsen) with bowel movements

Alarm Features (argue AGAINST IBS)

• First onset after age 40-50
• Progressive course
• Rectal bleeding
• Significant unexplained weight loss
• Nocturnal diarrhea
• Steatorrheal stools
• Persistent diarrhea despite 48-hour fast
• Anemia, elevated ESR/CRP, leukocytes/blood in stool
• Stool volume >200-300 mL/day
• Family history of colorectal cancer, IBD, or celiac disease

Differential Diagnosis

Diagnostic Workup

Minimal evaluation (no alarm features, typical presentation)

• CBC
• Fecal calprotectin or lactoferrin (to screen for IBD, especially in IBS-D)
• CRP (in IBS-D)
• Celiac serology (anti-tTG IgA + total IgA) in IBS-D populations where celiac prevalence ≥1%

Additional tests (when indicated)

• Stool ova and parasites (if endemic area or exposure history)
• Hydrogen breath test (lactose) or 3-week lactose-free trial
• Glucose hydrogen breath test (SIBO)
• Colonoscopy with random biopsies: indicated with alarm features, onset >40, or treatment failure; biopsies rule out microscopic colitis
• Upper GI endoscopy: for concurrent dyspepsia symptoms
• Abdominal ultrasound: if right upper quadrant pain suggests biliary disease

Treatment

Step 1: Education, Reassurance, Lifestyle

• Explain the functional/brain-gut nature of the disorder
• Identify and eliminate individual food triggers
• Stress management
• Exercise (low risk, overall benefit)
• Avoid nutritionally depleted diets

Step 2: Dietary Interventions

Low-FODMAP Diet (strongest dietary evidence)

1. Restriction phase (2-6 weeks): eliminate all 5 FODMAP subgroups
2. Reintroduction phase: challenge individual FODMAPs to identify personal triggers
3. Maintenance phase: personalized long-term diet

Fiber

• Soluble fiber (psyllium): effective for IBS-C; reduces perception of rectal distention
• Insoluble fiber (wheat bran): not supported by evidence, may worsen symptoms
• Start low, titrate slowly to 20-30 g/day total

Step 3: Symptom-Targeted Pharmacotherapy

For IBS-D (diarrhea-predominant)

For IBS-C (constipation-predominant)

For Abdominal Pain/Cramps (all subtypes)

Step 4: Psychological/Brain-Gut Behavioral Treatments

Prognosis

• IBS is a chronic, relapsing condition but is not associated with increased mortality or risk of IBD/colorectal cancer
• Subtypes can shift over time in the same patient
• ~30-40% of patients have symptom remission over years
• Quality of life impairment can be substantial
• Comorbid psychological disorders worsen prognosis

• Low-FODMAP diet is now the best-supported dietary intervention - superior to others in a 2025 network meta-analysis (PMID 40258374, Lancet Gastroenterol Hepatol)
• Brain-gut behavioral therapies (CBT, gut-directed hypnotherapy) confirmed effective in 2024-2025 network meta-analyses (PMID 38777133, PMID 41077057)
• Global IBS prevalence 4.1% by Rome IV in a 2025 meta-analysis of 2006-2024 data (PMID 40359286)

Hepatic Hemangioma

Overview

• No malignant potential - there has never been a reported case of malignant degeneration
• Extremely low risk of spontaneous rupture or hemorrhage (in contrast to hepatic adenoma)
• Most remain stable or grow very slowly over time

Gross Pathology

• Cavernous vascular spaces filled with blood
• Single layer of flat endothelial cells lining each space
• Fibrous stroma separating the spaces
• May contain organizing thrombi or calcifications
• Surrounded by a pseudocapsule formed by compressed liver parenchyma (not a true capsule)

Epidemiology and Demographics

• Prevalence: 5-20% of the general population
• Predominant in women aged 20-50
• Most patients have a single lesion (90%); 10% have multifocal disease
• Size ranges from millimeters to >10 cm
• Giant hemangioma: currently defined as >10 cm (the threshold was previously 5 cm)
• No estrogen receptors identified, but estrogen exposure (e.g., oral contraceptives, pregnancy) may lead to higher rates of enlargement without increased rupture risk

Clinical Presentation

Symptoms (when present)

• Vague abdominal pain or discomfort
• Early satiety
• Nausea and vomiting
• Fullness or pressure sensation in the right upper quadrant

Rare Complications

Imaging

Ultrasound

• Appearance: well-demarcated, homogeneous, hyperechoic (bright) lesion
• No posterior acoustic shadowing
• Most accurate for lesions <3 cm
• Contrast-enhanced ultrasound (CEUS): shows early peripheral nodular enhancement with progressive centripetal fill-in; avoids radiation and can be used when CT/MRI contrast is contraindicated

CT (Triple-phase/Multiphase)

1. Pre-contrast: well-defined, hypodense (hypointense) lesion
2. Arterial phase: early discontinuous peripheral nodular enhancement ("cotton wool" or "globular" enhancement)
3. Venous/delayed phases: progressive centripetal fill-in - contrast moves from periphery inward - with eventual isodense or hyperdense appearance ("fill-in pattern")

• Small hemangiomas (<1.5 cm) may fill in so rapidly that the nodular pattern is missed
• Large hemangiomas may show incomplete fill-in or central scarring/fibrosis

MRI

MRI with vascular contrast (gadolinium) is preferred over hepatobiliary contrast agents for hemangioma characterization.

Nuclear Medicine

• Technetium-99m-labeled red blood cell (RBC) scan: historically accurate but now rarely needed given high-quality CT/MRI availability

Summary: Imaging Algorithm

Incidentally found liver lesion
          ↓
   Ultrasound (first-line)
   Typical hyperechoic lesion < 3 cm in healthy patient?
          ↓ Yes                         ↓ Atypical / >3 cm / known malignancy
   Diagnosis secure                   Multiphase CT or MRI
   No further workup needed                 ↓
                                   MRI most accurate
                                   (sensitivity 90%, specificity ~100%)
                                        ↓ Still uncertain
                                   CEUS or surgical/biopsy

Differential Diagnosis

Management

Four Key Management Principles (Current Surgical Therapy, 14e)

1. The majority of hemangiomas, regardless of size, are asymptomatic and do not require intervention
2. Always consider a broad differential for symptoms in patients with incidentally found hemangioma - an alternative etiology is found in ~50% of cases
3. The ability to perform minimally invasive resection should not expand the indications for surgery
4. Operative treatment fails to improve symptoms in approximately 30-50% of carefully selected symptomatic patients

Observation (Standard for Most)

• Asymptomatic patients with secure diagnosis - no surveillance needed
• Asymptomatic patients regardless of lesion size
• Women of childbearing age - no need to stop OCP or modify pregnancy plans
• Small (<5 cm) lesions with typical imaging features

Routine surveillance imaging is not warranted in asymptomatic patients with a confirmed hemangioma.

Indications for Treatment (Narrow)

1. Severe persistent symptoms with no other identifiable etiology after thorough workup
2. Intraparenchymal or intraperitoneal hemorrhage (exceedingly rare; often associated with Kasabach-Merritt)
3. Biliary obstruction or hepatic venous compression (Budd-Chiari)
4. Diagnostic uncertainty with inability to exclude malignancy

Surgical Treatment

• Exploits the pseudocapsule as a natural dissection plane
• Incise Glisson's capsule adjacent to tumor, develop the peritumoral plane
• Preserves maximum functional liver parenchyma
• Vascular structures are displaced (not invaded) and can be preserved
• Associated with lower postoperative complication rates vs. formal resection
• Best for sublobar, peripheral hemangiomas

• Necessary for lobar hemangiomas or those involving central hepatic structures
• Ipsilateral hepatic artery ligation facilitates decompression
• Preoperative arterial embolization (day before) may be used for massive lesions

• Low central venous pressure anesthesia
• Pringle maneuver (hepatic inflow occlusion) for visualization
• Cell salvage/autotransfusion
• Laparoscopic or robotic approach preferred when feasible
• Operative mortality: <1%

Non-surgical Interventions

Pediatric Hemangiomas

• Account for ~12% of all childhood hepatic tumors
• Usually multifocal; may involve other organs
• Large lesions can cause congestive heart failure (arteriovenous shunting)
• Untreated symptomatic childhood hemangiomas carry high mortality
• Small capillary hemangiomas: almost all spontaneously resolve
• Treatment: embolization for symptoms; medical therapy for CHF; resection for rupture or failure of conservative measures

Lab Values

• LFTs: usually normal
• Tumor markers (AFP, CEA, CA19-9): normal
• In Kasabach-Merritt: thrombocytopenia, elevated FDPs, hypofibrinogenemia, prolonged clotting times

Prognosis and Natural History

• Benign course in the vast majority
• Most remain stable; slow growth may occur
• No malignant transformation - ever
• Spontaneous rupture: exceedingly rare
• Estrogen exposure may accelerate enlargement but does not increase rupture risk
• Excellent surgical outcomes when intervention is needed (mortality <1%)