A 44-year-old woman is admitted to the ICU 1 hour after having undergone a 3-hour abdominal operation for the debridement of infected necrotizing pancreatitis. The operation apparently resulted in 3500 mL of blood loss. She received approximately 4000 mL of crystalloid and 2 U packed red blood cell (PRBC) replacement during the operation. Prior to the procedure, the patient had been receiving imipenem and fluconazole for gram-negative bacteremia and fungemia. The patient’s skin appears cool and mottled. She is intubated and ventilated. Her vital signs are pulse 115 beats/min, blood pressure 85/60 mm Hg, and temperature 35.5°C (95.9°F). Her breath sounds are present bilaterally and her abdomen is soft and distended. A chest radiograph reveals bibasilar atelectasis. Electrocardiogram (ECG) reveals sinus tachycardia. Complete blood count reveals WBC 24,000/mm3, hemoglobin 12 g/dL, and hematocrit 40%.
What are the likely causes of this patient’s low blood pressure?
What should be the next steps in this patient’s management?
What are the best methods to provide ongoing assessment of this patient’s condition?
ANSWERS TO CASE 30: The Hypotensive Patient
Summary: A 44-year-old woman has recently undergone a 3-hour abdominal operation for the debridement of infected necrotizing pancreatitis and lost 3500 mL of blood. She received 4000 mL of crystalloid and 2 U PRBC during the operation. The patient had been receiving imipenem and fluconazole for gram-negative bacteremia and fungemia. She has poor skin perfusion, tachycardia, and hypotension.
• Likely causes of low blood pressure: Combined effects of inadequate resuscitation of blood loss and sepsis.
• Next steps in management: Fluid resuscitation. Consider blood transfusion if patient is a transient responder.
• Best methods to provide ongoing assessment: Place central venous pressure (CVP) monitor and arterial catheter for continuous blood pressure monitoring; consider echocardiography or pulmonary artery (PA) catheter placement to evaluate ventricular function and cardiac output; consider uncontrolled ongoing surgical blood loss if the patient fails to respond to resuscitation.
1. Recognize the presence and severity of hemorrhagic shock and understand the principles of early treatment.
2. Be able to describe the causes and treatment of postoperative hypotension.
3. Understand the principles of resuscitation, infection source control, and metabolic support for patients with sepsis.
This patient is exhibiting concerning signs of inadequate tissue perfusion with mottling and coolness of her extremities. Given her current situation, she likely has under-resuscitation of volume. In general, each unit of PRBC contains 250 to 300 mL in volume. In this patient, who in addition to blood loss from her operation and coagulopathy has systemic inflammatory response from pancreatitis and infection, the so-called normal amount of fluid loss from the intravascular space is further accentuated by pathological microvascular leak. A concerning factor in this patient’s case is the extremely bloody nature of her procedure that raises our clinical suspicion for potential inadequate control of intra-abdominal bleeding sources. To make matters even more complex, this patient has symptoms consistent with systemic infection such as leukocytosis, hypothermia, and a known history of gram-negative bacteremia and fungemia, therefore implicating sepsis as another potential cause of shock.
The initial approach is to begin resuscitation with crystalloid fluids and simultaneously begin close monitoring of response to resuscitative efforts. The patient’s clinical responses, including mentation, urine output, and peripheral circulation, should be closely assessed. In addition, CVP monitoring would be helpful to guide our endpoint of intravascular volume replacement. Because the primary therapeutic goals are to minimize the degree and duration of shock and correct the underlying cause, aggressive resuscitation should accompany diagnostic workup. In most cases, the initial approach to resuscitation for hypotension is to give crystalloid fluids (eg, normal saline, lactated Ringer solution). This will begin to stabilize the patient as the workup proceeds. Because this patient is clearly compromised physiologically and has a known history of systemic infection, it is important to bear in mind that uncontrolled infection could be a cause of the clinical picture; therefore, it would not be unreasonable to broaden her antimicrobial coverage after having obtained blood cultures. In this case, vancomycin should be considered preemptive coverage for resistant strains of gram-positive microbes.
APPROACH TO: The Hypotensive Patient
SHOCK: An acute clinical syndrome initiated by ineffective perfusion, resulting in injury and dysfunction in various organs systemically.
CENTRAL VENOUS CATHETER: An intravenous catheter of adequate length to measure pressures in the superior vena cava when placed via internal jugular vein or subclavian vein.
ECHOCARDIOGRAPHY: Ultrasonography that evaluates ventricular function, distension (or collapse) of the vena cava, and right heart. An experienced echocardiographer can also often accurately estimate the presence of pulmonary hypertension.
LACTATE: When this end product of anaerobic metabolism is elevated, it suggests a global deficit in oxygen delivery.
PA CATHETER: A catheter capable of measuring venous pressures that is placed in the pulmonary artery. The pressure measured, when inflow is blocked (by an inflated balloon), is extrapolated to be equal to the right atrial pressures because normally pulmonary vascular resistance is very low. This catheter can also measure cardiac output by the thermodilution method, thus permitting the clinician to track cardiac performance and response to interventions. Despite the theoretical advantages of PA catheter for the direction of perioperative care in the high-risk population, observations from the Canadian randomized controlled trial did not demonstrate benefits related to PA catheter–directed therapy.
Note: This extrapolated number and unsure nature of intravascular/intrathoracic pressures are two of the many drawbacks to routine use of the PA catheter.
Hypotension leading to shock can result from decreased intravascular volume, intrinsic cardiac pump dysfunction, and/or acute vasodilation without a concomitant increase in intravascular volume. Persistent hypotension results in lack of perfusion to organ systems and can lead to multiorgan system dysfunction and organ failure. A systematic approach is mandatory to minimize the length of time a patient is in shock. Consider the hemodynamic system as an arrangement of pump, pipes, and fluid volume. This simplistic idea translates to the three primary components of cardiovascular physiology: cardiac (pump), vascular tone (pipes), and intravascular volume (fluid). All components of the system need be intact to maintain normal perfusion. Malfunction of one or more components in the system may contribute to hypotension. Evaluation of a patient with postoperative hypotension should include a review of the pertinent history, a careful physical examination, vital signs and urine output, and review of administered medications.
Table 30–1 lists the differential diagnoses of common causes of hypotension in the perioperative period.
Table 30–1 • CLASSIFICATION OF SHOCK
Central venous monitoring or cardiac echocardiogram can provide valuable information concerning hypotension and help guide efforts at fluid resuscitation when the clinical picture is unclear; however, these diagnostic maneuvers should not be used to replace one’s clinical judgment. In a patient with previously normal renal function, urine output is often a reliable indicator of adequate resuscitation. Potential drawbacks of using urine output as the major endpoint of resuscitation may occur in hyperglycemic patients with falsely high urine output caused by glucose spillage in the urine, and the patient who may develop low urine output from acute renal insufficiency following severe or prolonged shock.
Monitoring and measurements of resuscitation endpoints include
• Foley catheter
• Central venous catheter for frequent CVP measurements
• Arterial catheter for continuous blood pressure monitoring (preferred) or frequent noninvasive blood pressure measurements
• Serial hemoglobin measurements
• Serial arterial blood gases (ABGs) for trends in lactate level or base deficit
Note: Early hemoglobin levels may not reflect active hemorrhage prior to the dilutional effect of crystalloid resuscitation.
Patients who respond initially to crystalloid resuscitation but then have a subsequent drop in arterial blood pressure may have ongoing surgical bleeding. An alternative cause is microvascular leak from systemic inflammatory mediators. In comparison to actively bleeding patients, those with microvascular leak syndrome show a more gradual decrease in blood pressure. In the setting in which hemorrhage is suspected and crystalloid only stabilizes the patient transiently, transfusion with PRBC is advised. In patients suspected of hemorrhage, a coagulation profile consisting of international normalized ratio (INR), partial thromboplastin time (PTT), and platelets should be checked to rule out nonsurgical sources of bleeding. Bleeding patients may continue to bleed as the result of coagulopathy or “medical causes” for bleeding. Resuscitation with PRBCs alone exacerbates coagulopathy in the bleeding patient because the clotting factors get further diluted. For this reason, it is important to resuscitate bleeding patients with red blood cells, fresh frozen plasma (FFP), and platelets. Recent military and civilian retrospective studies suggest that a ratio of 1 U of FFP should be transfused for every 1 to 1.5 U of PRBCs. Additionally, platelets and cryoprecipitate (rich in fibrinogen) are also important adjuncts in correcting or preventing coagulopathy. This approach to the resuscitation of the hypotensive, bleeding patient has been referred to as hemostatic resuscitation. Medical causes of bleeding are sometimes difficult to differentiate from anatomical bleeding causes when active bleeding is ongoing; therefore, the initial strategy is to address the “medical causes,” and then considered anatomic causes if bleeding continues after correction of the “medical causes.”
Often, the patient’s recent medical history suggests possible etiologies of hypotension. A thorough history and clinical examination will direct appropriate workups. Distributive causes for hypotension include any condition that causes acute vasodilation of the vascular space. This increase in the capacity of this vast network of vessels without a concomitant increase in intravascular fluid results in hypotension. The initial treatment for distributive shock involves fluid resuscitation to fill the increased volume of the vascular pool. Once this has begun, application of vasoconstrictive agents may be necessary to maintain a balance of normovolemia and pharmacologic vascular tone. If the etiology of the distributive shock is sepsis, treatment of the underlying infection with “source control” should accompany aggressive resuscitation. This may include broad-spectrum antimicrobial therapy and operative intervention to stabilize the systemic repercussions of infection.
Medications may also induce vasodilation. In a patient with mild to moderate hypovolemia, iatrogenic vasodilation with vasodilatory drugs can result in profound hypotension. It is important to remember that some drugs used for sedation, analgesia, and induction of anesthesia are vasodilators. Less commonly, anaphylaxis can accompany medication or blood product infusions. Hemodynamic support with epinephrine is often needed in acute anaphylactic shock.
Acute injury to the cervical or upper thoracic spinal cord can result in the loss of autonomic tone and produce acute hypotension (neurogenic shock). A hallmark of this type of hypotension is a normal or low heart rate in someone who is not on β-blockers.
Cardiogenic: Intrinsic and Extrinsic
Intrinsic conditions may include cardiogenic shock related to acute coronary syndrome in someone with preexisting cardiac disease. Conversely, classic extrinsic causes of cardiac function include tension pneumothorax that results in compression of the vena cava and right heart by a unilateral increasing intrathoracic pressure and shifting of the mediastinum away from the affected side. Another extrinsic cause is cardiac tamponade that limits right heart filling by compressing the thin-walled right ventricle and shifting the septum toward the more robust left ventricle, thus decreasing left ventricular end-diastolic volume.
A patient’s history and physical examination often suggest a primary diagnosis for hypotension and shock. There are patients, however, who present with combinations of causes for their hypotension. These patients can be a diagnostic dilemma and require more invasive methods for determining the source and management of their shock.
The PA catheter is an instrument that can give additional information in situations in which pump dysfunction is contributing to hypovolemic or septic shock. It may also prove beneficial in patients with acute renal failure where urine output cannot be used as an indication of normovolemia. Because of the placement-related and infectious complications associated with PA catheters, bedside echocardiography has largely replaced PA catheters for the bedside assessment of intravascular volume and cardiac functions in the critical care setting.
Restore oxygen delivery! This can be approached from an algorithm that evaluates and treats cardiogenic, distributive, and volume components of inadequate perfusion. First, there has to be adequate fluid volume in the system for perfusion. If vasodilation is contributing to a perceived hypovolemia in the presence of adequate fluid resuscitation, then and only then should vasoconstrictive agents (eg, norepinephrine, dopamine, Neo-Synephrine [phenylephrine], epinephrine, vasopressin) be considered. The specific etiology of the vasodilation will help determine which agent is most appropriate. If the primary problem is an intrinsic cardiac problem, augmentation of preload with gentle fluid resuscitation and addition of an inotrope may be the first step to stabilization. If there is an extrinsic cardiac problem such as tension pneumothorax or cardiac tamponade, these should be quickly decompressed with thoracostomy tube for the former and pericardiocentesis for the latter. If the etiology is mixed, a combination of the modalities just described may be needed. For these complex patients a bedside echocardiogram, or in some cases, a PA catheter may give the additional information needed to fine-tune diagnosis and management (Table 30–2).
Table 30–2 • HEMODYNAMIC VARIABLES IN DIFFERENT SHOCK STATES
30.1 A 65-year-old man is noted to have a blood pressure of 90/62 mm Hg on the evening after an uncomplicated small bowel resection for obstruction. His heart rate is 110 beats/min, respiratory rate 24 breaths/min, and temperature 37.4°C (99.3°F); urine output only 20 mL over 2 hours and oxygen saturation by pulse oximetry 95%. His preoperative hemoglobin level was 12.6 g/dL. Which of the following statements is most accurate regarding this patient?
A. A hemoglobin level performed in the recovery room after surgery of 12.4 g/dL is good evidence against active hemorrhage.
B. Intravenous furosemide (Lasix) should be administered.
C. This patient is most likely affected by anxiety and a mild anxiolytic and careful observation should be initiated.
D. Initial therapy should be intravenous crystalloid fluid bolus.
E. CT scan to assess for possible intra-abdominal bleeding or intra-abdominal septic source.
30.2 A 56-year-old woman is admitted to the intensive care unit (ICU) for ventilator management after an AAA repair. The patient is noted to have a urine output of 20 mL over 3 hours. Her blood pressure is 100/55 mm Hg, heart rate 110 beats/min, and temperature 35.6°C (96.1°F). Her serum troponin levels are elevated. Which of the following is the most likely diagnosis?
A. Intra-abdominal hemorrhage
B. Renal insufficiency
C. Neurogenic shock
D. Postsurgical hypothermia
E. Acute coronary syndrome with cardiogenic shock
30.3 A 51-year-old woman has undergone an open elective cholecystectomy 5 days previously. She has fever of 1-day duration and complains of shortness of breath and cough. Her pulse rate is 120 beats/min, temperature 39.5°C (103.1°F), respiratory rate 46 breaths/min, blood pressure 110/70 mm Hg, and O2 saturation level 89% on 60% O2 by face mask. She has crackles in the left lung base and her leukocyte count is 17,000 cells/mm3. Her chest radiograph shows left lower lobe subsegmental infiltrate. Which of the following is correct regarding this patient’s care?
A. A higher FIO2 should be avoided so oxygen toxicity is avoided.
B. Intravenous streptokinase for pulmonary embolus should be initiated.
C. Mechanical ventilation and transfer to the ICU are indicated.
D. A perinephric abscess is the most likely diagnosis.
E. Fluid restriction is indicated because her pulmonary examination suggests fluid overload.
30.4 Which of the following statements regarding fluid resuscitation is most accurate regarding volume repletion?
A. At equilibrium, approximately a third of administered crystalloid remains in the intravascular space.
B. Colloid resuscitation is preferable to crystalloid resuscitation in patients with acute blood loss.
C. PRBC should be transfused when hemoglobin values are less than 12 g/dL.
D. Hetastarch distributes to the extracellular space at equilibrium.
E. In patients with septic shock, resuscitation with blood products is preferable over fluids.
30.5 Which of the following statements best describes the difference between distributive shock and hemorrhagic shock?
A. Distributive shock requires treatment with vasoconstrictive agents only while hemorrhagic shock is treated with blood products and fluid repletion.
B. The transfusion of blood products improves hemorrhagic shock but is not indicated in distributive shock.
C. Both processes produce low urine output, but only hemorrhagic shock produces prerenal azotemia.
D. CVP measurement allows for the differentiation between distributive shock and hemorrhagic shock.
E. Distributive shock is always associated with normal or low heart rates.
30.1 D. This patient has hypotension, tachycardia, tachypnea, and low urine output following surgery. These are indicators of volume depletion. A normal hemoglobin level acutely does not accurately reflect volume status. The initial treatment should be intravenous crystalloid fluid resuscitation, and, if the intravascular volume of the patient is unclear, the patient would benefit from placement of CVP catheter for the assessment of intravascular volume status. Alternatively, bedside echocardiography can be obtained to determine intravascular status as well as cardiac function CT scans offer information regarding intra-abdominal infectious sources; however, in a patient who is immediate postoperative, the CT findings would be grossly abnormal and would not be helpful. CT scans could identify intra-abdominal fluid collection and could be useful in characterizing the fluid; however, it is not the preferred study to identify patients with active bleeding during the postoperative course.
30.2 E. Other causes are possible, however. The serum troponin elevation is highly suggestive of acute coronary syndrome or myocardial infarction. A 12-lead ECG and echocardiography should be obtained as adjunctive studies, which may provide valuable information to help direct subsequent fluid and pharmacologic therapy.
30.3 C. This patient has significant hypoxemia and tachypnea despite high levels of oxygen; this portends the possible need for mechanical ventilation. The differential diagnosis includes subphrenic abscess causing acute lung injury, postoperative pneumonia, and pulmonary embolism. Intravenous heparin (and not intravenous streptokinase) would be the treatment in pulmonary embolism.
30.4 A. At equilibrium, only a third of isotonic crystalloid remains in the intravascular space; thus 3 mL of crystalloids is usually infused for every 1 mL of blood lost. No clinical or laboratory evidence indicates an advantage of colloid over crystalloid for acute blood loss resuscitation. Hetastarch is a colloid solution and tends to remain in the intravascular space at equilibrium. The transfusion of blood products has been definitively proven to improve outcome in patients with large amount of blood loss. It is assumed that the transfusion of PRBC improves oxygen delivery to the tissues; however, because of storage-related changes in the PRBC, it remains unproven that blood transfusions improve oxygen consumption at the tissue level.
30.5 B. Transfusion of blood products helps replace the loss of volume, oxygen-carrying capacity, and clotting capacity associated with the blood loss due to hemorrhagic shock. Blood products administration may help improve the vital signs in patients with distributive shock based on the volume of the blood product, but in general, this is not the best method of addressing the volume depletion; intravenous crystalloid and vasopressor agents are the best treatment for distributive shock. Blood products should not be administered only for the purpose of volume resuscitation. Distributive shock includes septic shock, neurogenic shock, and anaphylactic shock. In the setting of neurogenic shock, the underlying cause is a loss of sympathetic tone that is often associated with bradycardia and hypotension. However, in the setting of septic shock and anaphylactic shock, central sympathetic discharge is intact; therefore the patients generally develop tachycardic responses to the low blood pressure.
The initial therapy for hypotension in most patients in whom sepsis is suspected should be aggressive fluid resuscitation—not vasopressors!
Source control in patients with a surgical infection frequently requires appropriate procedures to control infection (eg, drainage, debridement, bowel resection). For these types of patients, antibiotics alone are not usually adequate for source control.
Clinical measures of perfusion status are adequate in most patients for determination of the adequacy of resuscitation.
Invasive monitoring using PA catheterization should be considered when patients do not respond appropriately to initial therapy with stabilization of organ function and vital signs.
Do not be falsely reassured by a normal hemoglobin value in hypotensive surgical patients: They bleed whole blood!
Patients younger than 30 years with a good cardiac reserve and patients on β-blockers may not exhibit the expected tachycardia response to hemorrhage until late in the course of shock.
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