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Surgical Emergencies 

Surgical Emergencies
Chapter:
Surgical Emergencies
Author(s):

Maria D. Georgiades

, Stephen M. Luczycki

, and Linda L. Maerz

DOI:
10.1093/med/9780199377275.003.0011
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date: 24 October 2020

Bleeding after Carotid Endarterectomy

Definition

Bleeding from the carotid artery, internal jugular vein, smaller vessels, or raw tissue after carotid endarterectomy (CEA). Postoperative hemorrhage is rare (occurs in <1%–4% of patients).

Presentation

  • In the awake patient, anxiety may be the first symptom of early airway compromise. Neurologic symptoms may rarely occur as a result of compression or disruption of the internal carotid artery.

  • Tachycardia and tachypnea may occur, possibly due to anxiety. Decreased oxygen saturation is a late occurrence. Hypotension due to exsanguination from disruption of the suture line occurs rarely.

  • New onset of dysphonia and stridor are diagnostic of airway compromise.

  • An expanding hematoma may develop, which may or may not be pulsatile.

Anatomy and Pathophysiology

  • Sites of operative hemorrhage after CEA include both venous and arterial bleeding at sites remote from the carotid artery itself. Diffuse microvascular bleeding may be caused by residual heparin effect or effects of antiplatelet drugs. The suture line of the endarterectomy site is another potential source of bleeding, usually presenting as diffuse oozing from the wound. In those instances in which vein-patch angioplasty is employed, the patch may rupture. Arterial bleeding may result in exsanguinating hemorrhage.

  • An acute neck hematoma exerts pressure on the larynx and may cause life-threatening airway compromise.

Immediate Management of Acute Respiratory Distress

  • Increase FiO2 to 100%.

  • Elevate the head of the bed.

  • Immediate re-exploration is mandatory. Even a hematoma that initially appears benign can rapidly progress and compromise the airway. The surgical team should be called urgently to the bedside. Transport the patient to the operating room if the clinical situation permits.

  • If the patient is in acute respiratory distress, it may be necessary to evacuate the hematoma first in order to intubate the trachea. Open the skin incision to reduce pressure on the trachea.

  • If endotracheal intubation is impossible and airway obstruction is imminent, establishing a surgical airway may be necessary.

Differential Diagnosis

  • Anaphylaxis

  • Laryngeal edema

  • Acute pulmonary edema

  • Tension pneumothorax

  • Acute coronary syndrome

  • Pulmonary embolus

Diagnostic Studies

  • This is primarily a clinical diagnosis that is made by clinical course and physical examination. Maintain a high index of suspicion in patients who have undergone this procedure.

  • Because the patient can deteriorate rapidly, diagnostic studies (i.e., imaging) are not usually feasible. If the bleeding is slow and there is no acute airway compromise, carotid duplex ultrasound and diagnostic cervical ultrasound may be used to establish the diagnosis.

Subsequent Management

  • After a definitive airway is established, transport the patient to the operating room (OR) for exploration of the operative site.

  • Be prepared for a major vascular operation, including carotid isolation and repair.

Risk Factors

  • Surgical technique

  • Perioperative hypertension

  • Perioperative use of aspirin or other antiplatelet agents

  • Failure to reverse heparin with protamine sulfate

  • Postoperative anticoagulation with heparin or warfarin

  • The use of a small vein may increase the risk of rupture after a vein patch procedure.

Prevention

  • Meticulous hemostasis at the time of the original operation

  • Systolic blood pressure should be <140 mm Hg in normotensive patients and 160 mm Hg in chronically hypertensive patients.

  • Consider administering protamine (1–1.5 mg per 100 units of heparin, not to exceed 50 mg) to reverse heparin used during the procedure. This has been demonstrated to reduce postoperative bleeding complications without influencing the incidence of postoperative stroke.

  • The risk of vein patch rupture can be minimized by using greater saphenous vein harvested from the thigh.

Special Considerations

  • The incidence of reoperation for hematoma drainage is <1%, but this complication is potentially life-threatening because of associated airway compromise or, rarely, exsanguination from arterial suture line disruption.

Further Reading

Patel RB, Beaulieu P, et al. Share quality data are associated with increased protamine use and reduced bleeding complications after carotid endarterectomy in the Vascular Study Group of New England. J Vasc Surg. 2013; 58(6): 1518–1524.Find this resource:

Silva MB, Choi L, Cheng CC. Peripheral arterial occlusive disease. In: CM Townsend, RD Beauchamp, BM Evers et al, eds. Sabiston Textbook of Surgery. Philadelphia: Saunders; 2012:1763–1770.Find this resource:

Vaniyapong T, Chongruksut W, Rerkasem K. Local versus general anaesthesia for carotid endarterectomy. Cochrane Database Syst Rev. 2013; (12): CD000126.Find this resource:

Bleeding after Thyroid Surgery

Definition

Bleeding from the thyroid surface, dissected muscles, blood vessels in the vicinity of the thyroid gland, or the thyroid vessels themselves after thyroid surgery.

Presentation

  • In the awake patient, anxiety may be the first symptom of early airway compromise.

  • Tachycardia and tachypnea due to anxiety or airway compromise may occur. Decreased oxygen saturation is a late occurrence.

  • New onset of dysphonia and stridor indicate airway compromise.

  • A new neck mass in proximity to the operative site, which may or may not be associated with bleeding from the incision, represents a hematoma until proved otherwise.

Pathophysiology

  • Sources of postoperative hemorrhage after thyroid surgery include the raw surfaces of residual thyroid tissue, venous bleeding, and arterial bleeding. The bleeding may originate from vessels deep or superficial to the cervical strap musculature. Large goiters may also have associated enlarged mediastinal vessels, which include the internal mammary artery, the thyroidea ima artery, and the innominate vein.

  • When an acute hematoma occurs in the neck, the resulting pressure results in compression of the larynx, which can lead to life-threatening airway compromise.

  • Up to 3% of patients with thyroid diseases undergoing thyroid surgery have various acquired abnormalities of coagulation. The most common abnormality resembles von Willebrand disease. Patients who have hypothyroidism are the most likely to have an abnormal bleeding tendency, but coagulopathy may also occur in patients with thyroid malignancies.

Differential Diagnosis

  • Anaphylaxis

  • Laryngeal edema

  • Acute pulmonary edema

  • Tension pneumothorax

  • Acute coronary syndrome

  • Pulmonary embolus

Immediate Management

  • Increase FiO2 to 100%.

  • Immediate re-exploration is mandatory. Even a hematoma that initially appears benign can rapidly progress and compromise the airway. The surgical team should be called urgently to the bedside. Transport the patient to the OR if the clinical situation permits.

  • If endotracheal intubation is not possible and the patient is in acute distress, a laryngeal mask airway (LMA) may be attempted as a bridge to definitive airway management. Note: If the obstruction is infraglottic, an emergency surgical airway may be required.

  • After the hematoma is evacuated and laryngeal anatomy is restored, endotracheal intubation is usually possible. A surgical airway may rarely be necessary if endotracheal intubation is not possible after hematoma evacuation.

Diagnostic Studies

  • Physical examination and a high index of suspicion.

  • The urgency of the situation precludes imaging or other diagnostic studies.

Subsequent Management

After a definitive airway is established, the surgical site should be explored and the source of hemorrhage controlled.

Risk Factors

  • Surgical technique is the most common cause, particularly poor hemostasis.

  • Extensive surgery, which can include resection of large goiters

  • Underlying bleeding diathesis or the use of anticoagulants (e.g., heparin, warfarin, clopidogrel)

  • Male gender

  • Advanced age

Prevention

Meticulous hemostasis at the time of surgery. Preoperative coagulation screening to identify patients at increased risk of bleeding. Early detection and treatment of reversible coagulopathy. A drain can be placed in the resection bed to detect early signs of hemorrhage, especially if the patient is obese and body habitus makes it difficult to identify a cervical hematoma.

Special Considerations

  • Although bleeding and wound hematomas have an occurrence rate of <1%, these complications may be life-threatening due to airway compromise.

Further Reading

Bacuzzi A, Dionigi G, Del Bosco A, et al. Anaesthesia for thyroid surgery: perioperative management. Int J Surg. 2008; 6(Suppl 1): S82–S85.Find this resource:

Bergenfelz A, Jansson S, Kristoffersson A, et al. Complications to thyroid surgery: results as reported in a database from a multicenter audit comprising 3,660 patients. Langenbecks Arch Surg. 2008; 393: 667–673.Find this resource:

Chen AY, Bernet VJ, Carty SE, et al. American thyroid association statement on optimal surgical management of goiter. Thyroid. 2014; 24(2): 181–189.Find this resource:

Smith PW, Salomone LJ, Hanks JB. Thyroid. In: CM Townsend, RD Beauchamp, BM Evers, et al, eds. Sabiston Textbook of Surgery. Philadelphia: Saunders; 2012:886–923.Find this resource:

Facial Trauma

Definition

Maxillofacial injuries may be dramatic in appearance but are rarely life-threatening, unless airway, breathing, or circulation are compromised as a result of the injury.

Presentation

  • Compromise of airway and breathing:

    • Signs of impending respiratory obstruction include stridor, cyanosis, drooling, or ineffective gag reflex. Note: Airway obstruction may result in early death in the setting of multiple mandibular fractures or the combination of nasal, maxillary, and mandibular fractures.

    • Aspiration of teeth, blood, vomitus, or foreign bodies may cause airway obstruction or pneumonitis.

    • Patients may present with significant airway obstruction and impending respiratory failure despite normal pulse oximetry values.

  • Extensive hemorrhage:

    • Epistaxis

    • Scalp lacerations

    • Tongue lacerations

    • LeFort fractures

Anatomy and Pathophysiology

Blunt trauma may cause pan-facial fractures, significant soft tissue injury, and multiple remote sites of injury. Penetrating trauma ranges from simple lacerations to high-velocity missile injuries that may also involve the brain or neck.

Associated Injuries

  • Airway obstruction

  • Brain injury

  • Cervical spine injury

  • Hemorrhage from other sites

Immediate Management

  • Secure the airway: An emergency surgical airway may be necessary if orotracheal intubation is not possible. (Note: A cricothyroidotomy takes significantly less time than a tracheostomy and should be the surgical airway of choice if respiratory failure is imminent.) Nasotracheal intubation is contraindicated. If trained personnel are available and a cricothyroidotomy is not feasible, retromolar intubation or submental intubation may be considered.

  • Maintain cervical spine stabilization during airway management, with inline immobilization and minimal extension.

  • Establish large-bore peripheral intravenous access and begin fluid resuscitation.

  • Ask the surgical team to obtain local control of hemorrhage.

  • Assess the patient for concomitant injury.

Diagnostic Studies

A computed tomography (CT) scan is the standard of care. Three-dimensional reconstruction of axial CT sections should be requested if available. Panorex films are a useful adjunct for defining mandible fractures by providing a two-dimensional or linear image typically sufficient for diagnosis of fractures and operative planning.

Subsequent Management

  • Management of associated life-threatening injuries is undertaken first.

  • Early tracheostomy should be considered in selected patients as follows:

    • Pan-facial fractures

    • Profuse nasal bleeding

    • Severe soft tissue edema in the proximity of the airway

    • Patients with altered mental status

    • Severe facial burns

    • High spinal cord injuries

    • Difficult airway characteristics

    • Need for prolonged intubation

  • Assume that the cervical spine is unstable. A cervical collar should remain in place until definitive clearance by a combination of physical examination and radiographic examination.

  • Definitive management of facial injuries, particularly facial fractures, is usually delayed until life-threatening injuries are managed and the patient is stable.

Prevention

Maxillofacial injuries themselves are seldom life-threatening. Associated injuries, however, are serious and must be managed first in order to prevent loss of life.

Further Reading

Cappuccino GJ, Rhee ST, Granick MS. Maxillofacial injuries. In: JA Asensio, DD Trunkey (eds.). Current Therapy of Trauma and Critical Care. Philadelphia: Mosby; 2008:175–181.Find this resource:

Kellman RM, Rontal ML. Face. In: DV Feliciano, KL Mattox, EE Moore, eds. Trauma. New York: McGraw-Hill; 2013:395–413.Find this resource:

Pierre EJ, McNeer RR, Shamir MY. Early management of the traumatized airway. Anesthesiol Clin. 2007; 25(1): 1–11.Find this resource:

Vidya B, Cariappa KM, Kamath AT. Current perspectives in intraoperative airway management in maxillofacial trauma. J Maxillofac Oral Surg. 2012; 11(2): 138–143.Find this resource:

Laparotomy in the Critically Ill Patient

Definition

Emergency laparotomy in a critically ill patient for one or more life-threatening conditions, including infection, hemorrhage, ischemia, and abdominal compartment syndrome.

Presentation

  • Signs and symptoms vary with etiology and indication for laparotomy.

  • Shock (hemorrhagic, septic, or traumatic) is usually present.

  • End-organ perfusion may be impaired; signs include altered mental status, oliguria, tachypnea, hyperlactacidemia, and increased base deficit.

  • Significant tissue hypoperfusion can occur in spite of a normal arterial blood pressure. The presence of hypotension implies severe physiologic decompensation.

Pathophysiology

  • Shock is defined as the inadequate delivery of oxygen and nutrients to tissues as a result of hypoperfusion. Shock is characterized in various ways based on etiology. A clinically useful scheme is as follows:

    • Hypovolemic/hemorrhagic (acute hemorrhage of any etiology, peritonitis, pancreatitis, bowel obstruction)

    • Vasodilatory/distributive (sepsis, adrenal insufficiency, high spinal cord injury, liver failure, anaphylaxis)

    • Cardiogenic (myocardial infarction, tamponade, arrhythmias)

    • Obstructive (pulmonary embolus, pneumothorax)

    • Traumatic (a combination of hemorrhage, ischemia, reperfusion, activation of proinflammatory cascades)

  • Persistent hypothermia and progressive metabolic acidosis in the setting of massive transfusion are associated with life-threatening coagulopathy.

Differential Diagnosis

  • Cardiovascular collapse from an extraabdominal source of sepsis

  • Hemorrhage from extraabdominal trauma (pelvic fractures, long-bone fractures, thoracic injuries, open extremity wounds, scalp lacerations)

  • Massive myocardial infarction with acute cardiac failure and cardiovascular collapse

  • Massive pulmonary embolus with cardiovascular collapse

Immediate Management

  • Intubate the trachea and initiate mechanical ventilation. Consider etomidate (0.3 mg/kg IV) for induction if the patient is hemodynamically unstable. Sympathomimetic agents (e.g., ketamine) may cause profound hypotension in critically ill patients who have high circulating levels of endogenous catecholamines.

  • Increase FiO2 to maintain adequate oxygenation.

  • Be prepared to support the blood pressure. Hypotension is exacerbated by the transition from spontaneous ventilation to positive pressure mechanical ventilation.

  • Establish large-bore peripheral or central venous access.

  • Begin aggressive resuscitation with IV fluids. Transfuse with packed red blood cells (PRBCs) if indicated (i.e., for hemorrhagic shock).

  • Promptly identify and correct coagulopathy, thrombocytopenia, and platelet dysfunction.

  • Manage hypothermia.

  • Support blood pressure with vasopressors such as norepinephrine if indicated (septic shock).

  • Consider epinephrine infusion starting at 0.03–0.05 mcg/kg/min.

  • Begin broad-spectrum empiric or culture-directed antibiotic therapy (septic shock).

Diagnostic Studies

  • Abdominal and pelvic CT scan is the standard for diagnosis of intra-abdominal catastrophes.

  • If the patient is too unstable for CT scan, emergency surgery may be indicated based on a clinical diagnosis.

  • In the unstable trauma patient, focused abdominal sonography for trauma (FAST) and diagnostic peritoneal lavage can be quickly performed in the trauma bay to confirm intra-abdominal hemorrhage.

Subsequent Management

  • Maintain close communication with the surgical team throughout the perioperative period.

  • Hemodynamic instability may be caused by surgical manipulation and the patient’s underlying pathophysiology. A narcotic-based technique is associated with less vasodilation and negative inotropy and may be appropriate for patients who are hemodynamically unstable or who have underlying myocardial dysfunction. Pay close attention to the patient’s volume status, body temperature (fluid warmer, forced hot air blanket, elevated room temperature are most effective), and prevention of positioning injuries.

  • Patients undergoing emergency laparotomy are more likely to have hemodynamic instability in the postoperative period. Most patients remain intubated and mechanically ventilated after surgery until the patient has a stable pulmonary and hemodynamic status. Depending on the degree of physiologic impairment, many patients require prolonged mechanical ventilation and ongoing resuscitation in the ICU.

Risk Factors

  • The lethal triad: hypothermia, acidosis, coagulopathy

  • Advanced age

  • Chronic illness; comorbidities

Prevention

Early diagnosis of an impending intra-abdominal catastrophe before the patient goes into shock may prevent significant hypoperfusion and associated end-organ dysfunction, and may increase the likelihood of a good outcome.

Special Considerations

  • Intraoperative management of the critically ill patient is centered on maintaining oxygenation and perfusion. The choice of a specific technique is guided by the patient’s volume status and medical condition.

  • Abdominal compartment syndrome:

    • Abdominal hypertension with associated end-organ dysfunction (most commonly oliguria and elevated peak airway pressures)

    • Bladder pressure is used to estimate intra-abdominal pressure.

    • Etiologies include blunt and penetrating abdominal trauma, pelvic fractures, severe burns, massive resuscitation, and ischemia-reperfusion of the abdominal viscera.

    • Treatment is abdominal decompression, typically via decompressive laparotomy, leaving the abdomen open.

    • Mortality rates of 60%–70% reflect delayed diagnosis and underlying pathophysiology.

    • Early decompression is essential to prevent irreversible end-organ ischemia and cardiovascular collapse.

  • Damage control surgery:

    • Damage control is the preferred strategy for trauma patients with abdominal injuries complicated by hypothermia, coagulopathy, and acidosis. This strategy can also be used for critically ill nontrauma patients.

    • Assess physiologic reserve and severity of the physiologic insult.

    • Limited initial operation for the immediate control of hemorrhage and contamination; the abdomen is left open with a temporary abdominal closure in place.

    • Ongoing resuscitation and correction of physiologic derangements occurs in the ICU.

    • Subsequent operation for correction of anatomic abnormalities occurs in the stabilized patient, and early abdominal closure results in improved postoperative outcomes.

Further Reading

Asensio JA, McDuffie L, Petrone P, et al. Reliable variables in the exsanguinated patient which indicate damage control and predict outcome. Am J Surg. 2001; 182: 743–751.Find this resource:

Khan A, Hsee L, Mathur S, Civil I. Damage-control laparotomy in nontrauma patients: review of indications and outcomes. J Trauma Acute Care Surg. 2013; 75(3): 365–368.Find this resource:

Moayed O, Dutton RP. Anesthesia and acute care surgery. In: LD Britt, DD Trunkey, DV Feliciano, eds. Acute Care Surgery: Principles and Practice. New York: Springer; 2007:30–42.Find this resource:

Tiwari A, Haq AI, Myint F, et al. Acute compartment syndromes. Br J Surg. 2002; 89: 397–412.Find this resource:

Massive Hemorrhage

Definition

  • Major categories of massive hemorrhage include traumatic, gastrointestinal, and obstetric.

  • Classes of hemorrhagic shock:

    • Class I: blood loss up to 750 cc (up to 15% of blood volume)

      • Heart rate <100

      • Blood pressure normal

      • Pulse pressure normal or increased

    • Class II: blood loss 750–1500 cc (15–30% of blood volume)

      • Heart rate >100

      • Blood pressure normal

      • Pulse pressure decreased

    • Class III: blood loss 1500–2000 cc (30–40% of blood volume)

      • Heart rate >120

      • Blood pressure decreased

      • Pulse pressure decreased

    • Class IV: blood loss >2000 cc (>40% of blood volume)

      • Heart rate >140

      • Blood pressure decreased

      • Pulse pressure decreased

Presentation

  • Symptoms depend on the etiology of the hemorrhage. Gastrointestinal blood loss is typically painless; blood loss associated with trauma is associated with pain due to the injury.

  • Perturbation of vital signs depends on the degree of blood loss.

  • Severe shock is associated with cool, moist, pallid, or cyanotic skin. Mental status changes progress from anxiety to confusion to lethargy as the degree of shock progresses. Tachypnea occurs as the spontaneous minute ventilation increases in response to increasing metabolic demands. Oliguria is caused by renal hypoperfusion.

  • The source of hemorrhage may or may not be visible on external examination.

Pathophysiology

Hemorrhagic shock is a complex spectrum of events:

  • Acute massive blood loss resulting in circulatory collapse

  • Ischemia-reperfusion injury

  • Inflammatory and anti-inflammatory responses

  • Multiple organ dysfunction

Immediate Management

  • Intubate the trachea and initiate mechanical ventilation.

  • Establish large-bore peripheral and central IV access.

  • Transfuse with packed red blood cells and factors as indicated. Consider activating the massive transfusion protocol.

  • Begin resuscitation with crystalloid solutions (e.g., lactated Ringer’s solution or normal saline solution)

  • If laboratory studies are not feasible, resuscitate the patient with plasma, PRBCs, and platelets in a 1:1:1 ratio and minimal amounts of crystalloid solutions. Administer cryoprecipitate in the setting of continued microvascular bleeding.

  • If time permits, identify and correct specific deficits with serial prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR), fibrinogen, and platelet count. Elevated INR predicts the requirement for massive transfusion therapy.

Differential Diagnosis

Includes other causes of acute circulatory collapse:

  • Hypovolemic shock of nonhemorrhagic etiology (bowel obstruction, pancreatitis)

  • Vasodilatory/distributive shock

  • Obstructive shock

  • Cardiogenic shock

Diagnostic Studies

  • Gastrointestinal source: Endoscopy, interventional radiology, nuclear medicine.

  • Traumatic source: CT scan, FAST, diagnostic peritoneal lavage, immediate operative intervention in hemodynamically unstable patients.

  • Obstetric source: Usually apparent on physical examination or ultrasound examination.

Subsequent Management

  • Prompt surgical control of the bleeding.

  • Continue resuscitation throughout the perioperative period.

  • The goals of resuscitation are optimization of preload, cardiac performance, blood pressure, oxygen delivery and end-organ perfusion. No single parameter is universally applicable to every patient. Therefore, multiple endpoints should be optimized:

    • Clinical endpoints (heart rate, respiratory rate, blood pressure, urine output, level of consciousness, pulse pressure)

    • Cardiac output measurement

    • Metabolic parameters (lactate, base deficit)

    • Regional perfusion (gastric tonometry, sublingual capnography, near-infrared spectroscopy)

  • Massive transfusion protocols include component therapy, which replaces loss of blood volume, restores tissue perfusion, and corrects coagulopathy.

  • Fresh-frozen plasma produces less inflammation than do crystalloid or colloid solutions.

Risk Factors

  • GI source: Advanced age, comorbidities.

  • Traumatic source: Young age (injury is the leading cause of death for persons younger than 44 years of age in the US) and lifestyle issues.

  • Obstetric source: Postpartum hemorrhage is most commonly caused by uterine atony.

Prevention

Shock, hypoperfusion, and organ dysfunction are prevented by early control of the bleeding and appropriate resuscitation, regardless of the etiology of the hemorrhage.

Special Considerations

  • Massive transfusion is usually defined as the complete replacement of the patient’s entire blood volume—10 units PRBC—in a 24-hour period.

  • Role of recombinant-activated factor VII (rFVIIa):

    • Approved in the United States only for bleeding associated with hemophilia.

    • It is frequently used off-label, including for the reversal of the coagulopathy of trauma.

    • Generates a thrombin peak, which in turn causes formation of a fibrin plug.

    • May not be efficient in patients with acidosis (consider biochemical correction of acidosis prior to administration).

    • Hypothermia has little effect on efficacy.

Further Reading

Callcut RA, Cotton BA, Muskat P, et al. Defining when to initiate massive transfusion: a validation study of individual triggers in PROMMTT patients. J Trauma Acute Care Surg. 2013; 74(1): 59–65.Find this resource:

Duchesne JC, Heaney J, Guidry C, et al. Diluting the benefits of hemostatic resuscitation: a multi-institutional analysis. J Trauma Acute Care Surg. 2013; 75(1): 76–82.Find this resource:

Englehart M, Tieu B, Schreiber M. Endpoints of resuscitation. In: JA Asensio, DD Trunkey, eds. Current Therapy of Trauma and Critical Care. Philadelphia: Mosby; 2008:143–146.Find this resource:

Puyana JC, Tisherman SA, Peitzman AB. Current concepts in the diagnosis and management of hemorrhagic shock. In: JA Asensio, DD Trunkey, eds. Current Therapy of Trauma and Critical Care. Philadelphia: Mosby; 2008:437–445.Find this resource:

Spinella PC, Holcomb JB. Resuscitation and transfusion principles for traumatic hemorrhagic shock. Blood Rev. 2009; 23(6): 231–240.Find this resource:

Neck Injury

Definition

The neck contains a high density of vital structures located in a small and unprotected area. This may result in multisystem injury as a consequence of a single traumatic event.

Presentation

  • “Hard” signs warrant urgent surgical intervention:

    • Active bleeding

    • Expanding or pulsatile hematoma

    • Subcutaneous emphysema or air bubbling from wound

    • Airway compromise

    • Hematemesis

  • “Soft” signs warrant a more selective or expectant approach:

    • Dysphagia

    • Voice change

    • Hemoptysis

    • Wide mediastinum

Anatomy and Pathophysiology

  • Structures located in the neck:

    • Sternocleidomastoid muscles

    • Carotid artery, internal jugular vein, and vertebral artery

    • Pharyngeo-esophageal junction

    • Larynx and proximal trachea

    • Thyroid and parathyroid glands

    • Thoracic duct—enters the jugulosubclavian system in the left neck

    • Cervical vertebra and spinal cord

    • Long cervical musculature (posterior)

  • Anterior triangles of the neck: the area between the sternocleidomastoid muscles

  • Zones of the neck:

    • Zone I: the area bounded by the cricoid cartilage superiorly, the thoracic inlet inferiorly and the sternocleidomastoid laterally

    • Zone II: the area between the cricoid cartilage and the angle of the mandible

    • Zone III: the area bounded by the angle of the mandible inferiorly and the base of the skull superiorly

Associated Injuries

  • Spinal cord injury

  • Brain injury

  • Facial trauma

Immediate Management

  • Secure the airway if it is compromised. Orotracheal intubation is preferred; a surgical airway should be created if orotracheal intubation is not possible.

  • Maintain cervical spine stabilization during airway management.

  • Establish large-bore IV access. If central venous access is required, consider cannulating the femoral vein.

  • Resuscitate with crystalloid and PRBC if indicated.

  • Control active hemorrhage with local application of pressure. Balloon catheter tamponade may be required if manual pressure does not minimize hemorrhage while the patient is transported to the operating room.

Diagnostic Studies

  • Selected radiographic and endoscopic studies (see the following).

  • Immediate surgery in the setting of active hemorrhage.

Subsequent Management

  • Formal neck exploration is indicated in the presence of “hard” signs that indicate major vascular or aerodigestive tract injury.

  • Penetrating wounds should only be examined in the operating room as part of a formal neck exploration, and not in the emergency department.

  • In the absence of “hard” signs, a selective approach for management may be considered. This includes a thorough physical examination and specific diagnostic studies to identify vascular and aerodigestive tract injuries:

    • Esophagoscopy

    • Radiologic examination of the esophagus

    • Laryngoscopy/tracheoscopy/flexible nasoendoscopy

    • Arteriography (conventional and CTA)

    • Doppler ultrasonography

    • Computed tomography scan

  • Surgical treatment of identified injuries

  • Endovascular treatment of internal carotid injuries using stents and coils is gaining in acceptance. These techniques can often be used to treat the majority of vertebral artery injuries.

Special Considerations

Penetrating neck injuries are frequently life threatening. Immediate protection of the airway and rapid control of exsanguinating hemorrhage may be necessary.

Further Reading

Pierre EJ, McNeer RR, Shamir MY. Early management of the traumatized airway. Anesthesiol Clin. 2007; 25(1): 1–11.Find this resource:

Sperry JL, Moore EE, Coimbra R, et al. Western Trauma Association critical decisions in trauma: penetrating neck trauma. J Trauma Acute Care Surg. 2013; 75(6): 936–940.Find this resource:

Weireter LJ, Britt LD. Penetrating neck injuries: diagnosis and selective management. In: JA Asensio, DD Trunkey, eds. Current Therapy of Trauma and Surgical Critical care. Philadelphia: Mosby; 2008:197–206.Find this resource:

Ruptured Abdominal Aortic Aneurysm

Definition

Rupture is a potentially lethal complication of abdominal aortic aneurysm (AAA).

Presentation

  • Most patients who present with a ruptured AAA are unaware that they have aneurysmal disease. Patients may present with a symptomatic aneurysm (pain without evidence of rupture), a contained leak, or free rupture.

  • The classic clinical presentation of AAA rupture includes abdominal pain, hemodynamic instability, and a pulsatile abdominal mass. The abdominal pain is usually acute and unremitting, radiating to the back. If the rupture is in the retroperitoneum adjacent to the ureter, pain may be referred to the ipsilateral testicle or groin.

  • The patient may experience light-headedness or collapse because of acute hypovolemia.

  • If the aneurysm perforates into the duodenum or colon, massive gastrointestinal hemorrhage may occur.

  • If rupture occurs directly into the inferior vena cava, high-output congestive heart failure results.

Pathophysiology

Once an aneurysm develops, regardless of the etiology, enlargement is governed by the Law of Laplace, T = PR. T is tangential stress (which disrupts the wall of a sphere), P is the transmural pressure, and R is the radius. Large aneurysms are therefore more likely to rupture than small ones.

Immediate Management

  • Intubate the trachea if the patient is in severe shock and is unable to protect the airway.

  • If the clinical situation permits, transport the patient to the operating room and induce anesthesia after the patient is prepped and draped, because of the possibility of severe hypotension. Establish large-bore peripheral and central venous access.

  • Initiate aggressive resuscitation with IV fluids and PRBC.

  • Patients who present with the classic triad—pain, hemodynamic instability, and a pulsatile abdominal mass—must be transferred immediately to the operating room while being resuscitated. Any delay in control of the hemorrhage may be life threatening. Patients may undergo open or endovascular treatment.

Differential Diagnosis

  • Acute infectious or inflammatory abdominal process (hollow viscus rupture, ischemic or infarcted bowel, acute cholecystitis, acute pancreatitis) causing septic shock or exaggerated systemic inflammatory response

  • Hemorrhage from another intra-abdominal source, including ruptured visceral artery aneurysm, solid organ rupture (liver, spleen, kidney), hepatobiliary tumor hemorrhage

  • Massive gastrointestinal hemorrhage

  • Aortic dissection or aortic occlusion

  • Massive myocardial infarction with resultant acute cardiac failure, cardiogenic shock, and hemodynamic collapse

  • Massive pulmonary embolus with resultant obstructive shock and hemodynamic collapse

Diagnostic Studies

  • Hemodynamically stable patients should undergo CT of the abdomen and pelvis with intravenous contrast.

  • Duplex ultrasound (which may be performed at the bedside) can rapidly determine the presence of an AAA but may not image all portions of the aortic wall and therefore cannot identify ruptured versus nonruptured AAA.

Subsequent Management

  • All patients with ruptured AAA require urgent surgery or endovascular treatment.

  • Hemodynamically unstable patients must undergo immediate surgery or endovascular treatment. The patient is resuscitated during the surgical procedure because operative intervention cannot be delayed.

  • Assess and treat coagulopathy, thrombocytopenia, and platelet dysfunction. Baseline laboratory studies include CBC, PT, PTT, comprehensive chemistry panel, and cardiac enzymes. Coagulopathy is treated with fresh-frozen plasma and platelets, as indicated by laboratory parameters.

  • In hemodynamically stable patients, timing of the repair depends upon CT scan results. Emergency surgical management is necessary for a contained peritoneal rupture. In symptomatic patients who do not demonstrate CT evidence of rupture, repair can be postponed for up to 24 hours while the patient’s medical condition is optimized.

  • Endovascular repair (EVAR) has been demonstrated to decrease 30-day mortality and increase long-term survival for treatment of ruptured AAAs compared to open surgical repair. Although EVAR is associated with a decreased morbidity and mortality as compared to conventional surgery, there is an increased risk of reintervention. Depending on surgeon expertise, EVAR can be performed using local anesthesia for a percutaneous approach.

  • Monitor the patient for abdominal compartment syndrome after EVAR.

Risk Factors

  • The most important risk factor for rupture is the maximum diameter of the aneurysm. Aneurysms 4.0–5.4 cm in diameter have a yearly risk of rupture of 0.5–1%. Aneurysms 6–7 cm have a 6.6% risk of rupture per year.

  • Hypertension and hyperlipidemia

  • Chronic obstructive pulmonary disease

  • Smoking

  • Female gender

  • Eccentric saccular aneurysms

  • Rate of expansion of the AAA as an independent risk factor has been implicated but not proved.

Prevention

  • Avoid abrupt episodes of hypertension until the aneurysm has been secured.

  • The goal of elective repair of AAAs is to avoid rupture. The mortality of elective repair is 6% compared with >48% for repair of ruptured AAA. Endovascular repair confers a lower perioperative mortality rate (16%–31%) compared to open repair for ruptured AAA.

  • The overall mortality rate for ruptured AAA is 90%, since 60% of patients die prior to reaching the operating room.

  • Elective operative repair is recommended for AAAs 5.5 cm or greater in males and 4.5–5.0 cm in females and patients with greater than average rupture risk.

  • Rate of growth is an important indicator for surgical intervention, 5–7 mm per 6 months or >1 cm per year.

Special Considerations

  • More than 90% of aneurysms are associated with atherosclerosis, but 75% of patients with aneurysmal disease do not have occlusive vascular disease. Multiple factors contribute to the destruction of the media of the aortic wall, leading to aneurysm formation. Alterations in the connective tissue of the aortic wall, proteolytic enzymes, and inflammatory changes have been implicated.

  • Abdominal aortic aneurysms are less frequently caused by infection, arteritis, cystic medial necrosis, trauma, inherited connective tissue disorders, and pseudoaneurysm formation. Abdominal aortic aneurysms in young adults and children occur in the setting of tuberous sclerosis, Behcet disease, Marfan syndrome, Ehlers-Danlos syndrome, and infection associated with umbilical artery catheters.

Further Reading

Mehta M, Byrne J, et al. Endovascular repair of ruptured infrarenal abdominal aortic aneurysm is associated with low 30-day mortality and better 5-year survival rates than open surgical repair. J Vasc Surg. 2013; (2): 368–375.Find this resource:

Mehta M, Paty PS, et al. The impact of hemodynamic status on outcomes of endovascular abdominal aortic aneurysm repair for rupture. J Vasc Surg. 2013; 57(5): 1255–1260.Find this resource:

Norris EJ. Anesthesia for vascular surgery. In: RD Miller, ed. Miller’s Anesthesia, 7th ed. Philadelphia: Churchill Livingstone; 2010:1995–2006.Find this resource:

Tracci MC, Cherry KJ. Aorta. In: CM Townsend, RD Beauchamp, BM Evers et al, eds. Sabiston Textbook of Surgery. Philadelphia: Saunders; 2012:1697–1718.Find this resource:

Ruptured Ectopic Pregnancy

Definition

  • Implantation of a fertilized ovum outside of the endometrial cavity. In ruptured tubal ectopic pregnancy, trophoblastic proliferation extends through the tube. Hemorrhage occurs when the pregnancy extends into the large blood vessels in the broad ligament.

Presentation

  • Classic symptoms: Abdominal or pelvic pain and vaginal bleeding with an associated positive pregnancy test. Pain radiating to the shoulder, syncope, and shock are caused by hemoperitoneum secondary to ruptured ectopic pregnancy and occur in 20% of patients.

  • Hemorrhagic shock dependent on the degree of blood loss (see Massive Hemorrhage).

  • Abdominal tenderness in 90% of patients. Peritonitis in 70% (typically rebound tenderness). Cervical motion tenderness is present in approximately 30% of patients, whereas a tender adnexal mass is evident in up to 50%.

Pathophysiology

In tubal implantations (the most common type of ectopic gestation), the proliferating trophoblast first invades the luminal mucosa, then the muscularis and lamina propria, and finally the serosa. Invasion into the large blood vessels in the broad ligament results in hemorrhage that distorts the tube and causes pain. Although some ectopic pregnancies are clinically silent and end with spontaneous tubal abortion, rapid, life-threatening hemorrhage can occur.

Immediate Management

  • Establish large-bore peripheral IVs and/or central venous access.

  • Begin aggressive fluid resuscitation. Class I and Class II hemorrhagic shock can usually be treated with crystalloid infusions. Transfuse PRBCs in patients with Class III and Class IV shock (see Massive Hemorrhage).

Differential Diagnosis

  • Early diagnosis of hemorrhage is critical. The patient will not develop hypotension until 30% of the circulating blood volume is lost. Mild tachycardia may be the first sign of significant blood loss.

  • Infectious or inflammatory intra-abdominal and pelvic processes involving the gastrointestinal tract (perforated viscus, peptic ulcer disease, intestinal ischemia, appendicitis, colitis, cholecystitis, diverticulitis, pancreatitis), the urinary tract (urosepsis of any etiology, including pyelonephritis, cystitis, obstructive nephroureterolithiasis), and the reproductive tract (pelvic inflammatory disease, salpingitis, endometritis).

  • Hemorrhagic intra-abdominal and pelvic processes, including ruptured solid organ (liver, spleen, kidney), ruptured aortic or visceral aneurysm, ruptured hemorrhagic ovarian cyst, and uterine rupture (may occur with traumatic injury).

Diagnostic Studies

  • In patients who have hemorrhagic shock without a previous diagnosis of ectopic pregnancy, a single beta-hCG measurement and ultrasound guides definitive management.

  • Routine tests to establish ectopic pregnancy include serial measurements of beta-hCG, ultrasonography, uterine (endometrial) sampling, and occasionally progesterone levels.

Subsequent Management

  • Resuscitation is guided by CBC, PT, PTT, and INR. For massive hemorrhage, check baseline fibrinogen level and obtain periodic fibrinogen levels. Infusion of fresh-frozen plasma, cryoprecipitate, and platelets is guided by laboratory parameters and surgical bleeding.

  • Either laparotomy or laparoscopy with salpingectomy is performed for ruptured ectopic pregnancy.

  • If the patient is in severe hemorrhagic shock and rapid entry into the peritoneal cavity for source control is needed, emergency laparotomy is usually the best choice.

Risk Factors

  • High risk: Tubal surgery, tubal ligation, previous ectopic pregnancy, in utero exposure to diethylsilbestrol (altered fallopian tube development), presence of an intrauterine device, tubal pathology, assisted reproduction.

  • Moderate risk: Infertility, previous genital infections, multiple sexual partners.

  • Low risk: Previous pelvic infection, cigarette smoking, vaginal douching, young age at first intercourse.

Prevention

Risk stratification and a high index of suspicion can be used to diagnose an ectopic pregnancy before it ruptures and hemorrhages.

Special Considerations

  • The most common site of ectopic pregnancy is the fallopian tube (approximately 98% of all ectopic gestations). Abdominal, ovarian, and cervical ectopic pregnancies comprise the remaining 2%. Heterotopic pregnancy is the simultaneous occurrence of intrauterine and extrauterine gestation.

  • Serial beta-human chorionic gonadotropin (beta-hCG) levels are used in diagnostic algorithms. Progesterone levels are lower in ectopic pregnancies than in intrauterine gestations, but there is no established cutoff that can distinguish between the two.

  • Although multiple-dose systemic methotrexate is the first-line medical treatment of ectopic pregnancy, operative management is always the treatment of choice for a ruptured ectopic pregnancy.

Further Reading

Cohen A, Almog B, Satel A, et al. Laparoscopy versus laparotomy in the management of ectopic pregnancy with massive hemoperitoneum. Int J Gynaecol Obstet. 2013; 123(2): 263–272.Find this resource:

Seeber BE, Barnhart KT. Ectopic pregnancy. In: RS Gibbs, BY Karlan, AF Haney, et al, eds. Danforth’s Obstetrics and Gynecology. New York: Lippincott Williams & Wilkins; 2008:71–86.Find this resource:

Upper Gastrointestinal Bleeding

Definition

Upper gastrointestinal (UGI) hemorrhage originates proximal to the ligament of Treitz and accounts for almost 80% of major hemorrhage. Bleeding sites include the esophagus, stomach, duodenum, and, more rarely, the hepatobiliary tree, pancreas, and aortoenteric fistulae.

Presentation

  • Hematemesis and/or melena. Abdominal pain is rare.

  • Hemorrhagic shock. Classification is dependent on the degree of blood loss (see Massive Hemorrhage). Manifestations of shock, such as tachypnea, oliguria, and mental status changes may be present. In patients presenting with variceal hemorrhage, signs of portal hypertension and jaundice may be noted.

Anatomy and Pathophysiology

  • Peptic ulcer disease is the most common etiology of UGI hemorrhage and accounts for >50% of cases. Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are implicated in most cases.

  • Gastric and esophageal varices are the second most common etiology and account for 15% of cases of UGI hemorrhage. Cirrhosis causes portal hypertension, which in turn results in formation of varices.

  • Less common etiologies include stress ulceration, esophagitis, Mallory-Weiss tear, Dieulafoy’s lesion, arteriovenous malformations, and tumors. Unusual etiologies include hemobilia and hemosuccus pancreaticus; unlike most patients presenting with UGI hemorrhage, these patients may have abdominal pain. Aortoenteric fistula is another infrequent etiology of UGI hemorrhage.

  • The most predictive factors of severity include history of malignancy or cirrhosis, fresh blood hematemesis, hypovolemic signs including hypotension, tachycardia, shock, and Hb <8 g/dL at initial presentation.

Differential Diagnosis

Lower gastrointestinal hemorrhage originates below the ligament of Treitz and is generally less life threatening than UGI hemorrhage; shock is less likely and transfusion requirements are typically lower. Eighty percent of all patients with gastrointestinal hemorrhage pass blood in some form from the rectum. Twenty percent of all cases of apparent lower gastrointestinal hemorrhage have an upper gastrointestinal source, including massive nasal or oropharyngeal hemorrhage resulting in swallowed blood.

Immediate Management

  • Intubate the trachea and initiate mechanical ventilation if the patient has hematemesis or altered mental status, or if shock is imminent.

  • Be prepared to suction copious blood from the airway.

  • Establish large-bore peripheral and/or central venous access.

  • Resuscitate aggressively with crystalloid IV fluids and PRBC. Class I and Class II hemorrhagic shock usually can be treated with crystalloid infusions. Packed red blood cells are necessary in Class III and Class IV shock.

  • Draw baseline laboratories: CBC, PT, PTT, INR, and comprehensive metabolic panel, including liver function tests.

  • In cases of massive hemorrhage or known hepatic dysfunction, check fibrinogen level at baseline and periodically throughout the resuscitation.

  • Correct coagulopathy, thrombocytopenia, platelet dysfunction (medication induced or pathologic) with blood products and ddAVP.

Diagnostic Studies

  • After initial stabilization, determine the source of bleeding. Esophagogastroduodenoscopy is the modality of choice. Findings of bleeding peptic ulders are useful in predicting the risk of rebleeding:

  • Active arterial bleeding

    • 90%–100% risk of rebleeding without endoscopic intervention

    • 15%–30% risk of rebleeding with endoscopic intervention

  • Visible nonbleeding vessel

    • 40%–50% risk of rebleeding without endoscopic intervention

    • 15%–30% risk of rebleeding with endoscopic intervention

  • Adherent clot in ulcer base

    • 20%–30% risk of rebleeding without endoscopic intervention

    • 5% risk of rebleeding with endoscopic intervention

  • Angiography: Bleeding rates must be at least 0.5 mL/min for adequate visualization.

  • Nuclear medicine scans (tagged red blood cell scan): Bleeding rates must be at least 0.1 mL/min to be detected.

Subsequent Management

  • Interventional radiology may be used to deliver intra-arterial vasopressin or embolize the lesion in poor surgical candidates.

  • Restrictive transfusion strategies (threshold of Hb 7 g/dL) have beendemonstrated to decrease complications, transfusion requirements and mortality compared to liberal transfusion (threshold of Hb of 9 g/dL).

  • Surgical indications in patients with UGI hemorrhage attributable to peptic ulcer disease include two failed attempts of endoscopic hemostasis, rapid deterioration attributable to exsanguination, large visible vessels not amenable to endoscopic coagulation, and documented malignant ulcers.

  • Medical management of variceal hemorrhage includes vasopressin (bolus 0.4 U with 0.4–1 U/min infusion) plus nitroglycerin (10–50 mcg/min) or octreotide (50 mcg bolus with 50 mcg/h infusion for 5 days).

  • Endoscopic management of variceal hemorrhage includes sclerotherapy and variceal band ligation.

  • Esophageal variceal bleeding may be treated with transjugular intrahepatic portosystemic shunt (TIPS) when medical and endoscopic therapy fail or are not feasible, as a bridge to hepatic transplantation. There is an associated risk of worsening hepatic encephalopathy.

Risk Factors for Mortality (6%–10%)

  • Advanced age

  • Renal insufficiency

  • Hepatic failure

  • Disseminated malignancy

Prevention

Treatment of Helicobacter pylori infection and limitation of NSAID use may help to prevent complications of peptic ulceration. Major indications for stress ulcer prophylaxis in the critically ill include respiratory failure and coagulopathy.

Special Considerations

  • In general, 80% of cases of UGI hemorrhage stop spontaneously. Ninety percent hemostasis rates are achieved with endoscopic therapy. Surgical indications in patients with UGI hemorrhage attributable to peptic ulcer disease include two failed attempts of endoscopic hemostasis, rapid deterioration attributable to exsanguination, large visible vessels not amenable to endoscopic coagulation, and documented malignant ulcers. In patients with UGI hemorrhage and cirrhosis, prophylactic antibiotics have been demonstrated to reduce bacterial infections and increase survival. Norfloxacin 400 mg BID for 7 days has been recommended.

Further Reading

Cheung FK, Lau JY. Management of massive peptic ulcer bleeding. Gastroenterol Clin North Am. 2009; 38(2): 231–243.Find this resource:

Khamaysi I, Gralneck IM. Acute upper gastrointestinal bleeding (UGIB)-initial evaluation and management. Best Pract Res Clin Gastroenterol. 2013; 27(5): 633–638.Find this resource:

Donahue PE. Foregut. In: LD Britt, DD Trunkey, DV Feliciano, eds. Acute Care Surgery: Principles and Practice. New York: Springer; 2007:450–470.Find this resource:

Sass DA, Chopra KB. Portal hypertension and variceal hemorrhage. Med Clin North Am. 2009; 93(4): 837–853.Find this resource:

Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013; 368(1): 11–21.Find this resource: