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HEMORRHAGE - A Surgical Perspective

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1. DEFINITION

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2. ETIOLOGY

A. Traumatic

• Penetrating injuries (stab wounds, gunshot wounds)
• Blunt trauma with organ laceration (liver, spleen, kidney)
• Fractures (pelvic fractures - major cause of retroperitoneal hemorrhage; long bone fractures)
• Surgical/iatrogenic injury to major vessels

B. Spontaneous / Pathological

• Vessel wall disease: Atherosclerosis, aneurysm rupture, vasculitis, Marfan syndrome
• Coagulation disorders: Hemophilia A & B, von Willebrand disease, thrombocytopenia (ITP, DIC)
• Anticoagulant therapy: Warfarin, heparin, DOACs, aspirin, NSAIDs
• Infections: Erosion of vessel walls by septic processes (mycotic aneurysm, abscess)
• Neoplasms: Tumor invasion of vessels
• Peptic ulcer disease: Erosion into gastroduodenal/left gastric artery
• Esophageal varices: Portal hypertension
• Aortoenteric fistula
• Hemorrhagic diathesis / haemophilia - even minor injuries can be fatal

C. Factors That Worsen Hemorrhage

• Rise in blood pressure during recovery from shock
• Muscular movements loosening a blood clot
• Sepsis causing erosion of vessel walls
• Partial transection of an artery (retraction cannot occur, so bleeding is greater than with complete transection)

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3. PATHOGENESIS - FLOW CHART

BLOOD LOSS FROM VASCULAR COMPARTMENT
            |
            v
  DECREASED CIRCULATING BLOOD VOLUME
            |
     ________|________
    |                 |
    v                 v
BARORECEPTOR     CHEMORECEPTOR
ACTIVATION        STIMULATION
(aortic arch,    (hypoxia, acidosis,
 carotid bodies)  CO2 changes)
    |                 |
    |_________________|
            |
            v
   SYMPATHETIC NERVOUS SYSTEM ACTIVATION
   + Hypothalamic-Pituitary-Adrenal Axis
            |
      _______|_______
     |       |       |
     v       v       v
 Catecho-  Renin-  Vasopressin
 lamines   Angiotensin  Release
 Released  Cascade
     |       |       |
     |_______|_______|
            |
            v
   PERIPHERAL VASOCONSTRICTION
   + Increased Heart Rate & Contractility
   + Fluid Retention (oliguria)
   + Blood Flow Preferentially to Heart & Brain
            |
            v
  [IF HEMORRHAGE CONTINUES / EXCEEDS COMPENSATION]
            |
            v
   DECREASED TISSUE PERFUSION
  /         |          \         \
 v          v           v         v
Parenchymal Endothelial  Cellular  Metabolic
Cell Injury  Activation/ Hypoxia   Acidosis
            Microvascular
            Damage
             |           |
             v           v
        Cellular      Intracellular
        Aggregation   Fluid Loss +
                      ↓ Coronary
                      Perfusion
             \___________/
                   |
                   v
          ↓ VENOUS RETURN
                   |
                   v
          FURTHER ↓ TISSUE PERFUSION
            (VICIOUS CYCLE OF SHOCK)
                   |
                   v
            IRREVERSIBLE SHOCK
              (Multi-Organ Failure, Death)

• The goal is to maintain perfusion to heart and brain at the expense of other organs
• Initial stimulus: loss of circulating blood volume
• Magnitude: proportional to both the volume and rate of blood lost
• Afferent signals from baroreceptors, chemoreceptors, and pain receptors converge in the CNS
• Efferent response: expands plasma volume, maintains peripheral perfusion, restores homeostasis

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4. CLASSIFICATION

A. By Timing (Clinical Classification - Bailey & Love / Surgical Tradition)

B. By Source of Vessel

C. By Location

D. By Severity - ATLS Classification (Schwartz's Surgery, Table 5-5)

Note: Young, healthy patients may maintain near-normal blood pressure until sudden cardiovascular collapse. Elderly patients on beta-blockers or anticoagulants tolerate much less. A systolic BP < 110 mmHg is now considered a clinically relevant threshold for hypoperfusion (Eastridge et al.).

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5. CLINICAL FEATURES

Early/Compensated Stage (Class I-II, <30% blood loss)

• Tachycardia (most sensitive early sign)
• Cool, clammy extremities
• Pallor
• Mild anxiety or restlessness
• Orthostatic hypotension
• Mild tachypnea

Decompensated Stage (Class III-IV, >30% blood loss)

• Hypotension (SBP < 90-100 mmHg; now < 110 mmHg is considered significant)
• Marked tachycardia (HR > 110-120 bpm)
• Confusion, agitation, or obtundation
• Absent or weak peripheral pulses
• Oliguria / anuria
• Severe pallor, cold sweating
• Rapid, shallow breathing

Features by Location

• External hemorrhage: Visible bleeding from wounds, open fractures
• Hemothorax: Decreased breath sounds, dullness to percussion, dyspnea
• Hemoperitoneum: Abdominal distension, tenderness, guarding, rigidity
• Retroperitoneal: Flank bruising (Grey Turner sign), pelvic tenderness; often occult
• Intracranial: Headache, vomiting, altered GCS, focal neurology
• Cardiac tamponade: Beck's triad - hypotension + raised JVP + muffled heart sounds (even 300-400 mL blood in pericardial sac is fatal)

Key point: Substantial volumes of blood may be lost before classic manifestations of shock appear. "When a patient is significantly tachycardic or hypotensive, this represents both significant blood loss AND physiologic decompensation." - Schwartz's Surgery

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6. DIAGNOSIS

Clinical Assessment

• History: mechanism of injury, anticoagulant use, bleeding disorders
• Vital signs: tachycardia, hypotension, tachypnea
• Physical exam: site of external bleeding, abdominal/thoracic signs, GCS

Laboratory Investigations

Note: Lactate and base deficit both correlate with shock severity but interestingly do not firmly correlate with each other - evaluation of both is useful.

Imaging

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7. TREATMENT

Immediate Priorities (in order)

A. Hemorrhage Control

• Direct sustained pressure to wound
• Tourniquets for extremity bleeding not controlled by pressure (apply in pre-hospital setting)
• Wound packing with hemostatic agents (Combat gauze)
• Proximal vascular control

• Direct compression + proximal vascular isolation and clamping
• For aortic injury: supraceliac aortic compression - retract stomach caudally, mobilize left lobe of liver, divide gastrohepatic ligament, compress aorta against vertebrae
• Hands-free aortic control: incise peritoneum, separate limbs of right diaphragmatic crus, apply aortic clamp
• Endovascular balloon occlusion of aorta (REBOA) - for patients with femoral arterial access
• Venous injury: compression + direct suture repair

• For multiple bleeding sites, coagulopathy, hypothermia - abbreviated "damage control" laparotomy
• Pack and temporize, achieve hemostasis, close abdomen temporarily
• Return to ICU for resuscitation, then definitive repair

• For pelvic fracture hemorrhage, hepatic/splenic hemorrhage in stable patients
• Identifies arterial source and occludes with coils or gelfoam

B. Damage Control Resuscitation (Current Strategy - Schwartz's Surgery)

• Target SBP 80-90 mmHg in penetrating injuries
• Prevents renewed bleeding from recently clotted vessels
• For blunt injury with head injury: SBP ≥ 110 mmHg (hypotension worsens brain injury)
• Aggressive crystalloid resuscitation to normalize BP is counterproductive - increases bleeding and mortality

• Resuscitate with blood products, NOT crystalloids
• Ratio: Packed Red Blood Cells : Fresh Frozen Plasma : Platelets = 1:1:1
• Early use of FFP to correct coagulopathy
• Massive transfusion protocol (MTP) activated for estimated blood loss > 10 units PRBCs/24h
• Cryoprecipitate for fibrinogen replacement (fibrinogen < 150 mg/dL)
• Recombinant Factor VIIa in refractory coagulopathic bleeding

• Hypothermia - warm IV fluids, warm OR, warming blankets; aim temp > 35°C
• Acidosis - control with hemorrhage control + resuscitation; bicarbonate rarely indicated
• Coagulopathy - treat with FFP, platelets, cryo; avoid dilutional coagulopathy

• Antifibrinolytic agent
• Give within 3 hours of injury (CRASH-2 trial) - reduces mortality
• 1 g IV over 10 min, then 1 g over 8 hours

• Only after adequate volume replacement
• Norepinephrine first-line for refractory vasodilatory shock

C. Surgical Procedures by Source

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8. COMPLICATIONS

Early Complications

Late Complications

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Key Clinical Pearls (Surgical)

1. Tachycardia alone is unreliable - only 65% of hypotensive hemorrhagic shock patients had tachycardia in one study; it was present in only 59% of those needing > 5 units pRBC.
2. "Hypotension begins at 110 mmHg" - a SBP < 110 mmHg correlates with increasing mortality in trauma hemorrhage (Eastridge et al.).
3. Partial arterial transection bleeds MORE than complete transection - because retraction and spasm cannot occur.
4. The abdomen can hide enormous blood volumes - physical exam is unreliable; use FAST/CT/DPL.
5. Damage control resuscitation - permissive hypotension + 1:1:1 blood products + early surgical hemorrhage control is the current standard of care.
6. Time is survival - each 3-minute delay in the ED increases mortality by approximately 1% in patients needing emergency laparotomy for hemorrhage.

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HEMORRHOIDS - A Surgical Perspective

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1. DEFINITION

• Right anterior
• Right posterior
• Left lateral

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2. ANATOMY

• Above dentate line: internal hemorrhoids (covered by insensate anorectal mucosa, visceral innervation - painless unless thrombosed/strangulated)
• Below dentate line: external hemorrhoids (covered by anoderm, richly innervated by somatic nerves - painful when thrombosed)

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3. ETIOLOGY

Predisposing Factors

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4. PATHOGENESIS - FLOW CHART

PREDISPOSING FACTORS
(Low fiber diet, constipation, straining, pregnancy,
 obesity, prolonged sitting, aging, portal hypertension)
            |
            v
INCREASED INTRA-ABDOMINAL / INTRARECTAL PRESSURE
            |
      _______|_______
     |               |
     v               v
VENOUS ENGORGEMENT    WEAKENING OF
OF HEMORRHOIDAL       ANCHORING CONNECTIVE
PLEXUS                TISSUE (Treitz muscle,
                      Parks ligament)
     |               |
     |_______________|
            |
            v
   ENGORGEMENT + LOSS OF MUCOSAL FIXATION
            |
      _______|________
     |       |        |
     v       v        v
BLEEDING   PROLAPSE   THROMBOSIS
(Bright     (Grade    (External or
red blood   I - IV)   Incarcerated
per rectum)           internal)
     |       |        |
     v       v        v
PAINLESS   MUCOID     PAIN,
HEMATOCHEZIA DISCHARGE SWELLING,
           PRURITUS   NECROSIS
                |
                v
          STRANGULATION
          (Grade IV - irreducible,
           vascular compromise)
                |
                v
            GANGRENE

• Normal: Hemorrhoidal cushions are supported by the internal sphincter, Treitz muscle, and Parks ligament
• Disease: Repeated straining and engorgement cause downward displacement ("sliding") of the cushions
• Venous engorgement leads to enlargement
• Disruption of the mucosal suspensory ligament (Parks ligament) allows prolapse
• Once prolapsed, the mucosa is exposed to the environment, causing mucoid discharge, irritation, and pruritus

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5. CLASSIFICATION

A. Anatomical Classification

B. Grading of Internal Hemorrhoids (Classic Goligher Classification)

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6. CLINICAL FEATURES

Symptoms

• Painless bright red rectal bleeding - hallmark symptom; blood drips or squirts into toilet bowl, coats stool (does not mix with it); usually occurs with defecation
• Prolapse - tissue protruding from anus (grades II-IV)
• Mucoid discharge - from exposed mucosa of prolapsed hemorrhoids
• Pruritus ani - from mucoid discharge irritating perianal skin
• Feeling of incomplete evacuation or anal discomfort
• Pain - only if thrombosis or strangulation occurs (severe, constant)

• Pain and swelling - sudden onset of painful perianal mass; most commonly due to acute thrombosis
• Perianal lump - tense, bluish, tender swelling at anal verge
• Itching and hygiene difficulty if skin tags are large (skin tags = fibrotic residua of prior thrombosed external hemorrhoids)
• Bleeding - less common; occurs if thrombosis erodes skin

• Circumferential prolapse, edematous, dark red or purple
• Severe constant pain
• Unable to be reduced
• Can progress to necrosis / gangrene

Signs on Examination

• Skin tags at anal verge
• Externally visible prolapsed hemorrhoids (grades III-IV)
• Thrombosed external hemorrhoid: tense, bluish, tender perianal mass

• Internal hemorrhoids are NOT palpable (soft and compressible)
• Important to rule out other anorectal pathology

• Definitive visualization of internal hemorrhoids
• Hemorrhoids bulge into the lumen when patient strains
• Appearance: purple-red vascular cushions at 3, 7, 11 o'clock positions

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7. DIAGNOSIS

Clinical Diagnosis

• History of painless bright red PR bleeding, prolapse, mucoid discharge, pruritus
• Examination: inspection, DRE, anoscopy, proctoscopy

Key Investigations

Differential Diagnosis (Important - Must Exclude)

Important: Hemorrhoids should never be assumed to be the cause of rectal bleeding in patients over 40 without colonoscopic exclusion of colorectal cancer.

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8. TREATMENT

STEP 1: Conservative / Medical Management (All Grades, First Line)

• High-fiber diet - 25-35 g/day; psyllium or methylcellulose supplement
• Increased fluid intake - 8 or more glasses of water per day; reduce caffeine and alcohol
• Stool softeners - docusate sodium
• Bowel habit modification - avoid straining; reduce time on toilet to < 3 minutes; no reading/phone on toilet
• Warm sitz baths - 2-3 times daily; reduces edema and soothes
• Topical agents - witch hazel (cotton application), topical hydrocortisone or -caine preparations (temporary symptomatic relief only - do not reduce hemorrhoids long-term)
• Phlebotonics - flavonoids (e.g., diosmin, hesperidin); improve venous tone, reduce inflammation, decrease bleeding and pruritus

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STEP 2: Office-Based (Non-Operative) Procedures

1. Rubber Band Ligation (RBL) - Most Common Office Procedure

• Indication: Grade I, II, III internal hemorrhoids
• Contraindicated in: patients on anticoagulants, antiplatelet therapy, or latex allergy
• Technique: Mucosa 1-2 cm proximal to dentate line is grasped and pulled into rubber band applier; band strangulates underlying tissue → fibrosis → prevents bleeding/prolapse
• Only 1-2 quadrants banded per session (spaced 3-4 weeks apart)
• Complications: Pain if band placed too close to dentate line; urinary retention (~1%); vasovagal reaction; thrombosis of external hemorrhoid; delayed bleeding (7-10 days when pedicle sloughs); necrotizing infection (rare but life-threatening - presents with severe pain + fever + urinary retention - requires urgent exam under anesthesia, debridement, broad-spectrum antibiotics)
• Success rate > 90%

2. Sclerotherapy (Injection Therapy)

• Indication: Grade I, II hemorrhoids; safe for patients on anticoagulants
• Sclerosants: 5% phenol in almond oil, hypertonic saline, ethanolamine, sodium morrhuate, quinine urea
• Technique: 1-3 mL injected into submucosa of hemorrhoid at 1 cm above dentate line; all 3 hemorrhoids may be treated in one session
• Mechanism: Sclerosis → shrinkage → fibrosis → fixation
• Complications: Injection into muscle (pain, ulceration, sloughing); infection; fibrosis

3. Infrared Photocoagulation (IRC)

• Indication: Grade I, II hemorrhoids
• Infrared energy applied at apex of hemorrhoid → coagulation → thrombosis → tissue destruction → scarring/fixation
• 3-4 applications per hemorrhoid; all 3 treated in one session
• Well tolerated; similar side effects to RBL

4. HET Bipolar System

• Grade I, II hemorrhoids
• Specialized forceps grasp hemorrhoid; bipolar energy applied
• Well tolerated

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STEP 3: Operative Treatment

A. Closed Submucosal Hemorrhoidectomy (Ferguson / Parks Hemorrhoidectomy)

• Most common technique
• Patient in prone jackknife or lithotomy position
• Elliptical incision from just distal to anal verge proximally to anorectal ring
• Internal sphincter fibers identified and preserved (not injured)
• Apex of hemorrhoidal plexus ligated; hemorrhoid excised
• Wound closed with running absorbable suture
• All three hemorrhoidal cushions may be removed; must preserve adequate perianal skin bridges to prevent anal stenosis

B. Open Hemorrhoidectomy (Milligan-Morgan Technique)

• Same excision as above, but wounds left open to heal by secondary intention
• Traditional technique; used widely in UK
• Slower healing but lower risk of wound infection

C. Whitehead's Hemorrhoidectomy

• Circumferential excision of all hemorrhoidal cushions just proximal to dentate line
• Largely abandoned due to risk of ectropion (Whitehead's deformity) - rectal mucosa pulled down to anal verge

D. Procedure for Prolapse and Hemorrhoids (PPH) / Stapled Hemorrhoidopexy

• Best suited for Grade II-III internal hemorrhoids
• Stapling device removes a ring of mucosa and submucosa proximal to the dentate line
• Mechanism: pexies redundant hemorrhoidal tissue + ligates venules feeding hemorrhoidal plexus + fixes redundant mucosa proximally
• Advantages: less postoperative pain and disability; shorter recovery
• Complications: chronic anal pain, bacteremia, rectovaginal fistula, obstructing rectal stricture, rectal perforation
• Recurrence rate slightly higher than excisional hemorrhoidectomy

E. Doppler-Guided Hemorrhoidal Artery Ligation (DGHAL) / Trans-Anal Hemorrhoidal Dearterialization (THD)

• Doppler probe identifies the feeding artery/arteries
• Vessels are ligated
• Less invasive; early results promising; long-term durability still being assessed

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Special Situations

Acute Thrombosed External Hemorrhoid

• Present within first 72 hours: Elliptical excision under local anesthesia in outpatient/office setting (simple incision and drainage is rarely effective as clot is loculated)
• After 72 hours: clot begins to resorb; pain resolves spontaneously; conservative management with sitz baths and analgesics sufficient; excision unnecessary

Acute Hemorrhoidal Crisis (Circumferential Prolapse)

• Circumferential prolapsed, thrombosed, incarcerated internal and external hemorrhoids ± necrosis
• Without necrosis: Inject mixture of 1% lidocaine with epinephrine + normal saline + hyaluronidase into all edematous tissues; massage; pressure dressing
• With necrosis: Emergency hemorrhoidectomy

Postpartum Hemorrhoids

• Hemorrhoidectomy is often the treatment of choice, especially in patients with chronic hemorrhoidal symptoms

Portal Hypertension + Hemorrhoids

• Hemorrhoidal disease is NOT more common in portal hypertension
• Rectal varices (distinct from hemorrhoids) may develop and bleed
• Treatment of rectal varices: lower portal venous pressure (pharmacologic/TIPS); rarely suture ligation
• Surgical hemorrhoidectomy should be avoided in portal hypertension due to bleeding risk

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9. COMPLICATIONS

Complications of Hemorrhoidal Disease

Complications of Rubber Band Ligation

Complications of Hemorrhoidectomy

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Summary Treatment Algorithm

SYMPTOMATIC HEMORRHOIDS
         |
         v
GRADE I + II
         |
         +--> Conservative: High fiber + fluids + sitz baths + avoidance of straining
         |             |
         |         If fails
         |             v
         |    Office-based: RBL (preferred) / Sclerotherapy / IRC
         |
GRADE III
         |
         +--> Office-based: RBL (first line)
         |             |
         |         If fails
         |             v
         |    Operative: Ferguson / Milligan-Morgan / PPH / DGHAL
         |
GRADE IV / STRANGULATED / MIXED
         |
         +--> Operative Hemorrhoidectomy (Ferguson or Milligan-Morgan)
         |
ACUTE THROMBOSED EXTERNAL (<72 hr)
         |
         +--> Elliptical Excision under local anesthesia

ACUTE THROMBOSED EXTERNAL (>72 hr)
         |
         +--> Conservative: sitz baths + analgesics

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