SHOCK IN SURGERY

HOSSEIN BOLOURIAN
“SHOCK IS THE MANIFESTATION OF THE RUDE UNHINGING OF THE
MACHINERY OF LIFE.”
—SAMUEL V. GROSS, 1872
 IS THE FAILURE TO MEET THE METABOLIC NEEDS
OF THE CELL AND THE CONSEQUENCES THAT
ENSUE.

THE INITIAL CELLULAR INJURY THAT OCCURS IS

REVERSIBLE; HOWEVER, THE INJURY WILL BECOME
IRREVERSIBLE IF TISSUE PERFUSION IS PROLONGED
OR SEVERE ENOUGH SUCH THAT, AT THE CELLULAR
LEVEL, COMPENSATION IS NO LONGER POSSIBLE.

MOST NOTABLY, OUR COMPREHENSION OF THE

SYMPATHETIC AND NEUROENDOCRINE STRESS
RESPONSES ON THE CARDIOVASCULAR SYSTEM
HAS FLOURISHED
• THE GENERAL APPROACH TO THE
MANAGEMENT OF PATIENTS IN
SHOCK HAS BEEN EMPIRIC
1. ASSURING A SECURE AIRWAY
WITH ADEQUATE
VENTILATION
2. CONTROL OF HEMORRHAGE
IN THE BLEEDING PATIENT
3. RESTORATION OF VASCULAR
VOLUME
4. TISSUE PERFUSION.
• THIS IMBALANCE BETWEEN CELLULAR SUPPLY AND DEMAND LEADS TO
NEUROENDOCRINE AND INFLAMMATORY RESPONSES, THE MAGNITUDE OF WHICH IS
USUALLY PROPORTIONAL TO THE DEGREE AND DURATION OF SHOCK.
• THE SPECIFIC RESPONSES WILL DIFFER BASED ON THE ETIOLOGY OF SHOCK
• FOR EXAMPLE, THE CARDIOVASCULAR RESPONSE DRIVEN BY THE SYMPATHETIC NERVOUS
SYSTEM IS MARKEDLY BLUNTED IN NEUROGENIC OR SEPTIC SHOCK

• MANY OF THE ORGAN-SPECIFIC RESPONSES ARE AIMED AT MAINTAINING PERFUSION IN

THE CEREBRAL AND CORONARY CIRCULATION
• THESE ARE REGULATED AT MULTIPLE LEVELS INCLUDING (A) STRETCH RECEPTORS AND
BARORECEPTORS IN THE HEART AND VASCULATURE (CAROTID SINUS AND AORTIC
ARCH), (B) CHEMORECEPTORS, (C) CEREBRAL ISCHEMIA RESPONSES, (D) RELEASE OF
ENDOGENOUS VASOCONSTRICTORS, (E) SHIFTING OF FLUID INTO THE INTRAVASCULAR
SPACE, AND (F) RENAL REABSORPTION AND CONSERVATION OFSALT AND WATER.
 FORMS OF SHOCK

• HYPOVOLEMIC/HEMORRHAGIC
 THE MOST COMMON CAUSE OF SHOCK IN THE SURGICAL OR TRAUMA PATIENT IS LOSS
OF CIRCULATING VOLUME FROM HEMORRHAGE.
 INCREASE VASOCONSTRICTION AND PERIPHERAL ARTERIAL RESISTANCE.
 INDUCES SYMPATHETIC STIMULATION, LEADING TO EPINEPHRINE AND
NOREPINEPHRINE RELEASE
 ACTIVATION OF THE RENIN ANGIOTENSIN CASCADE, AND INCREASED VASOPRESSIN
RELEASE
 LACK OF SYMPATHETIC EFFECTS ON CEREBRAL AND CORONARY VESSELS AND LOCAL
AUTOREGULATION PROMOTE MAINTENANCE OF CARDIAC AND CNS BLOOD FLOW
THE CLINICAL AND PHYSIOLOGIC RESPONSE TO HEMORRHAGE HAS BEEN CLASSIFIED
ACCORDING TO THE MAGNITUDE OF VOLUME LOSS.
1. LOSS OF UP TO 15% OF THE CIRCULATING VOLUME (700 TO 750 ML FOR A 70-KG
PATIENT) MAY PRODUCE LITTLE IN TERMS OF OBVIOUS SYMPTOMS.
2. WHILE LOSS OF UP TO 30% OF THE CIRCULATING VOLUME (1.5 L) MAY RESULT IN MILD
TACHYCARDIA, TACHYPNEA, AND ANXIETY.
3. HYPOTENSION, MARKED TACHYCARDIA (I.E., PULSE GREATER THAN 110 TO 120 BPM),
AND CONFUSION MAY NOT BE EVIDENT UNTIL MORE THAN 30% OF THE BLOOD
VOLUME HAS BEEN LOST.
4. LOSS OF 40% OF CIRCULATING VOLUME (2 L) IS IMMEDIATELY LIFE THREATENING
AND GENERALLY REQUIRES OPERATIVE CONTROL OF BLEEDING

YOUNG HEALTHY PATIENTS WITH VIGOROUS COMPENSATORY MECHANISMS MAY TOLERATE LARGER VOLUMES OF BLOOD LOSS WHILE
MANIFESTING FEWER CLINICAL SIGNS DESPITE THE PRESENCE OF SIGNIFICANT PERIPHERAL HYPOPERFUSION. THESE PATIENTS MAY
MAINTAIN A NEAR-NORMAL BLOOD PRESSURE UNTIL A PRECIPITOUS CARDIOVASCULAR COLLAPSE OCCURS. ELDERLY PATIENTS MAY BE
TAKING MEDICATIONS THAT EITHER PROMOTE BLEEDING (E.G., WARFARIN OR ASPIRIN), OR MASK THE COMPENSATORY RESPONSES TO
BLEEDING (E.G., Β-BLOCKERS). IN ADDITION, ATHEROSCLEROTIC VASCULAR DISEASE, DIMINISHING CARDIAC COMPLIANCE WITH AGE,
INABILITY TO ELEVATE HEART RATE OR CARDIAC CONTRACTILITY IN RESPONSE TO HEMORRHAGE, AND OVERALL DECLINE IN
PHYSIOLOGIC RESERVE DECREASE THE ELDERLY PATIENT’S ABILITY TO TOLERATE HEMORRHAGE.

RECENT DATA IN TRAUMA PATIENTS SUGGEST THAT A SYSTOLIC BLOOD PRESSURE (SBP) OF LESS THAN 110 MMHG IS A CLINICALLY
RELEVANT DEFINITION OF HYPOTENSION AND HYPOPERFUSION BASED UPON AN INCREASING RATE OF MORTALITY BELOW THIS
PRESSURE

SERUM LACTATE AND BASE DEFICIT ARE MEASUREMENTS THAT ARE HELPFUL TO BOTH ESTIMATE AND MONITOR THE EXTENT OF
BLEEDING AND SHOCK. SEVERAL STUDIES HAVE DEMONSTRATED THAT THE INITIAL SERUM LACTATE AND SERIAL LACTATE LEVELS ARE
RELIABLE PREDICTORS OF MORBIDITY AND MORTALITY WITH HEMORRHAGE FOLLOWING TRAUMA

ALTHOUGH HEMATOCRIT CHANGES MAY NOT RAPIDLY REFLECT THE TOTAL VOLUME OF BLOOD LOSS, ADMISSION HEMATOCRIT HAS
BEEN SHOWN TO BE ASSOCIATED WITH 24 HOUR FLUID AND TRANSFUSION REQUIREMENTS AND MORE STRONGLY ASSOCIATED WITH
PRBC TRANSFUSION THAN EITHER TACHYCARDIA, HYPOTENSION, OR ACIDOSIS.
MANAGEMENT OF TRAUMA PATIENTS, UNDERSTANDING THE PATTERNS OF INJURY OF
THE PATIENT IN SHOCK WILL HELP DIRECT THE EVALUATION AND MANAGEMENT.
PATIENTS WITH PENETRATING WOUNDS IS RELATIVELY SIMPLE BECAUSE POTENTIAL
BLEEDING SOURCES WILL BE LOCATED ALONG THE KNOWN OR SUSPECTED PATH OF
THE WOUNDING OBJECT. PATIENTS WITH PENETRATING INJURIES WHO ARE IN SHOCK
USUALLY REQUIRE OPERATIVE INTERVENTION.
PATIENTS WHO SUFFER MULTISYSTEM INJURIES FROM BLUNT TRAUMA HAVE MULTIPLE
SOURCES OF POTENTIAL HEMORRHAGE. BLOOD LOSS SUFFICIENT TO CAUSE SHOCK IS
GENERALLY OF A LARGE VOLUME, AND THERE ARE A LIMITED NUMBER OF SITES THAT
CAN HARBOR SUFFICIENT EXTRAVASCULAR BLOOD VOLUME TO INDUCE HYPOTENSION
(E.G., EXTERNAL, INTRATHORACIC, INTRA-ABDOMINAL, RETROPERITONEAL, AND LONG
BONE FRACTURE)
IN THE NON TRAUMA PATIENT, THE GI TRACT MUST ALWAYS BE CONSIDERED AS A SITE
FOR BLOOD LOSS.
• PLEURAL CAVITY CAN HOLD 2 TO 3 L OF BLOOD AND CAN THEREFORE BE A SITE
OF SIGNIFICANT BLOOD LOSS DIAGNOSTIC AND THERAPEUTIC TUBE
THORACOSTOMY MAY BE INDICATED IN UNSTABLE PATIENTS BASED ON
CLINICAL FINDINGS AND CLINICAL SUSPICION. IN A MORE STABLE PATIENT, A
CHEST RADIOGRAPH MAY BE OBTAINED TOLOOK FOR EVIDENCE OF
HEMOTHORAX.
• MAJOR RETROPERITONEAL HAEMORRHAGE TYPICALLY OCCURS IN ASSOCIATION
WITH PELVIC FRACTURES, WHICH IS CONFIRMED BY PELVIC RADIOGRAPHY IN
THE RESUSCITATION BAY.
• INTRAPERITONEAL HEMORRHAGE IS PROBABLY THE MOST COMMON SOURCE OF
BLOOD LOSS THAT INDUCES SHOCK THE PHYSICAL EXAM FOR DETECTION OF
SUBSTANTIAL BLOOD LOSS OR INJURY IS INSENSITIVE AND UNRELIABLE; LARGE
VOLUMES OF INTRAPERITONEAL BLOOD MAY BE PRESENT BEFORE PHYSICAL
EXAMINATION FINDINGS ARE APPARENT.
 TREATMENT

• CONTROL OF ONGOING HEMORRHAGE IS AN ESSENTIAL COMPONENT OF THE RESUSCITATION OF THE

PATIENT IN SHOCK
• PATIENTS WHO FAIL TO RESPOND TO INITIAL RESUSCITATIVE EFFORTS SHOULD BE ASSUMED TO HAVE
ONGOING ACTIVE HEMORRHAGE FROM LARGE VESSELS AND REQUIRE PROMPT OPERATIVE INTERVENTION.
• THE APPROPRIATE PRIORITIES IN THESE PATIENTS ARE AS FOLLOWS: (A) CONTROL THE SOURCE OF BLOOD
LOSS, (B) PERFORM IV VOLUME RESUSCITATION WITH BLOOD PRODUCTS IN THE HYPOTENSIVE PATIENT,
AND(C) SECURE THE AIRWAY.
• IN TRAUMA, IDENTIFYING THE BODY CAVITY HARBOURING ACTIVE HEMORRHAGE WILL HELP FOCUS
OPERATIVE EFFORTS; HOWEVER, BECAUSE TIME IS OF THE ESSENCE, RAPID TREATMENT IS ESSENTIAL, AND
DIAGNOSTIC LAPAROTOMY OR THORACOTOMY MAY BE INDICATED.
• MANAGEMENT STRATEGY KNOWN AS DAMAGE CONTROL RESUSCITATION. THIS
STRATEGY BEGINS IN THE EMERGENCY DEPARTMENT, CONTINUES INTO THE
OPERATING ROOM, AND INTO THE INTENSIVECARE UNIT (ICU). INITIAL
RESUSCITATION IS LIMITED TO KEEP SBP AROUND 80 TO 90 MMHG. THIS
PREVENTS RENEWED BLEEDING FROM RECENTLY CLOTTED VESSELS.
• THE INCREASE IN MORTALITY WITH HYPOTENSION IN THE SETTING OF BRAIN
INJURY MUST BE AVOIDED. IN THIS SETTING, A SBP OF 110 MMHG WOULD SEEM
TO BE MORE APPROPRIATE.
• REASONABLE CONCLUSIONS IN THE SETTING OF UNCONTROLLED HEMORRHAGE
INCLUDE
 (A) DELAY IN SURGERY FOR CONTROL OF HEMORRHAGE INCREASES MORTALITY;
 (B) WITH UNCONTROLLED HEMORRHAGE, ATTEMPTING TO ACHIEVE NORMAL BLOOD
PRESSURE MAY INCREASE MORTALITY, PARTICULARLY WITH PENETRATING INJURIES
AND SHORT TRANSPORT TIMES;
 (C) A GOAL OF SBP OF 80 TO 90 MMHG MAY BE ADEQUATE IN THE PATIENT WITH
PENETRATING INJURY
 (D) PROFOUND HEMODILUTION SHOULD BE AVOIDED BY EARLY TRANSFUSION OF RED
BLOOD CELL

• HYPOTHERMIA, ACIDOSIS, COAGULOPATHY

 CARDIOGENIC SHOCK
• CARDIOGENIC SHOCK IS DEFINED CLINICALLY AS CIRCULATORY PUMP FAILURE LEADING
TO DIMINISHED FORWARD FLOW AND SUBSEQUENT TISSUE HYPOXIA
• HEMODYNAMIC CRITERIA INCLUDE SUSTAINED HYPOTENSION (I.E., SBP<90 MMHG FOR
AT LEAST 30 MINUTES), REDUCED CARDIAC INDEX(<2.2 L/MIN PER SQUARE METER), AND
ELEVATED PULMONARY ARTERY WEDGE PRESSURE (>15 MMHG).
• MORTALITY RATES FOR CARDIOGENIC SHOCK ARE 50% TO 80%.
• ACUTE, EXTENSIVE MI IS THE MOST COMMON CAUSE OF CARDIOGENIC SHOCK
• SIGNS OF CIRCULATORY SHOCK INCLUDE HYPOTENSION, COOL AND MOTTLED SKIN,
DEPRESSED MENTAL STATUS, TACHYCARDIA, AND DIMINISHED PULSES
• CONFIRMATION OF A CARDIAC SOURCE FOR THE SHOCK REQUIRES
ELECTROCARDIOGRAM AND URGENT ECHOCARDIOGRAPHY
 TREATMENT

• INTUBATION AND MECHANICAL VENTILATION

• ADEQUATE OXYGENATION TO ENSURE ADEQUATE MYOCARDIAL O2 DELIVERY AND JUDICIOUS FLUID
ADMINISTRATION TO AVOID FLUID OVERLOAD AND DEVELOPMENT OF CARDIOGENIC PULMONARY
EDEMA
• ELECTROLYTE ABNORMALITIES, COMMONLY HYPOKALEMIA AND HYPOMAGNESEMIA, SHOULD BE
CORRECTED
• PAIN IS TREATED WITH IV MORPHINE SULFATE OR FENTANYL
• SIGNIFICANT DYSRHYTHMIAS AND HEART BLOCK MUST BE TREATED WITH ANTIARRHYTHMIC
DRUGS, PACING, OR CARDIOVERSION
• WHEN PROFOUND CARDIAC DYSFUNCTION EXISTS, INOTROPIC SUPPORT MAY BE INDICATED TO
IMPROVE CARDIAC CONTRACTILITY AND CARDIAC OUTPUT.
 SEPTIC SHOCK (VASODILATORY SHOCK)

• IN THE PERIPHERAL CIRCULATION, PROFOUND VASOCONSTRICTION IS THE TYPICAL

PHYSIOLOGIC RESPONSE TO THE DECREASED ARTERIAL PRESSURE AND TISSUE
PERFUSION WITH HEMORRHAGE, HYPOVOLEMIA, OR ACUTE HEART FAILURE. THIS IS NOT
THE CHARACTERISTIC RESPONSE IN VASODILATORY SHOCK.
• VASODILATORY SHOCK IS THE RESULT OF DYSFUNCTION OF THE ENDOTHELIUM AND
VASCULATURE SECONDARY TO CIRCULATING INFLAMMATORY MEDIATORS AND CELLS OR
AS A RESPONSE TO PROLONGED AND SEVERE HYPOPERFUSION.
• VASODILATORY SHOCK IS CHARACTERIZED BY PERIPHERAL VASODILATION WITH
RESULTANT HYPOTENSION AND RESISTANCE TO TREATMENT WITH VASOPRESSORS
• DESPITE THE HYPOTENSION, PLASMA CATECHOLAMINE LEVELS ARE ELEVATED, AND THE
RENIN-ANGIOTENSIN SYSTEM IS ACTIVATED IN VASODILATORY SHOCK.
• THE MOST FREQUENTLY ENCOUNTERED FORM OF VASODILATORY SHOCK IS SEPTIC SHOCK.
• MANIFESTATIONS OF SEPSIS MAY BE EVIDENT. THESE FINDINGS INCLUDE ENHANCED CARDIAC
OUTPUT, PERIPHERAL VASODILATION, FEVER, LEUKOCYTOSIS, HYPERGLYCEMIA, AND
TACHYCARDIA.
• VASODILATORY SHOCK SEEMS TO REPRESENT THE FINAL COMMON PATHWAY FOR PROFOUND
AND PROLONGED SHOCK OF ANY ETIOLOGY.
• FEVER, TACHYCARDIA, AND TACHYPNEA, SIGNS OF HYPOPERFUSION SUCH AS CONFUSION,
MALAISE, OLIGURIA, OR HYPOTENSION MAY BE PRESENT. THESE SHOULD PROMPT AN
AGGRESSIVE SEARCH FOR INFECTION, INCLUDING A THOROUGH PHYSICAL EXAMINATION,
INSPECTION OF ALL WOUNDS, EVALUATION OF INTRAVASCULAR CATHETERS OR OTHER FOREIGN
BODIES, OBTAINING APPROPRIATE CULTURES, AND ADJUNCTIVE IMAGING STUDIES, AS NEEDED.
 TREATMENT

• FLUID RESUSCITATION AND RESTORATION OF CIRCULATORY VOLUME WITH BALANCED SALT SOLUTIONS IS ESSENTIAL.
FLUID RESUSCITATION SHOULD BEGIN WITHIN THE FIRST HOUR AND SHOULD BE AT LEAST 30 ML/KG FOR HYPOTENSIVE
PATIENTS.
• EMPIRIC ANTIBIOTICS MUST BE CHOSEN CAREFULLY BASED ON THE MOST LIKELY PATHOGENS (GRAM-NEGATIVERODS,
GRAM-POSITIVE COCCI, AND ANAEROBES)
• VASOPRESSORS MAY BE NECESSARY TO TREAT PATIENTS WITH SEPTIC SHOCK. CATECHOLAMINES ARE THE VASOPRESSORS
USED MOST OFTEN, WITH NOREPINEPHRINE BEING THE FIRST-LINE AGENT FOLLOWED BY EPINEPHRINE
• HYPERGLYCEMIA AND INSULIN RESISTANCE ARE TYPICAL IN CRITICALLY ILL AND SEPTIC PATIENTS, INCLUDING PATIENTS
WITHOUT UNDERLYING DIABETES MELLITUS.
• THE USE OF CORTICOSTEROIDS IN THE TREATMENT OF SEPSIS AND SEPTIC SHOCK HAS BEEN CONTROVERSIAL FOR
DECADES.
•
 NEUROGENIC SHOCK

• NEUROGENIC SHOCK REFERS TO DIMINISHED TISSUE PERFUSION AS A RESULT OF LOSS OF VASOMOTOR TONE TO
PERIPHERAL ARTERIAL BEDS.
• NEUROGENIC SHOCK IS USUALLY SECONDARY TO SPINAL CORD INJURIES FROM VERTEBRAL BODY FRACTURES OF THE
CERVICAL OR HIGH THORACIC REGION THAT DISRUPT SYMPATHETIC REGULATION OF PERIPHERAL VASCULAR TONE
• ACUTE SPINAL CORD INJURY MAY RESULT IN BRADYCARDIA, HYPOTENSION, CARDIAC DYSRHYTHMIAS, REDUCED
CARDIAC OUTPUT, AND DECREASED PERIPHERAL VASCULAR RESISTANCE.
• THE CLASSIC DESCRIPTION OF NEUROGENIC SHOCK CONSISTS OF DECREASED BLOOD PRESSURE ASSOCIATED WITH
BRADYCARDIA (ABSENCE OF REFLEXIVE TACHYCARDIA DUE TO DISRUPTED SYMPATHETIC DISCHARGE), WARM
EXTREMITIES (LOSS OF PERIPHERAL VASOCONSTRICTION), MOTOR AND SENSORY DEFICITS INDICATIVE OF A SPINAL
CORD INJURY, AND RADIOGRAPHICEVIDENCE OF A VERTEBRAL COLUMN FRACTURE
 TREATMENT

• FLUID RESUSCITATION AND RESTORATION OF INTRAVASCULAR VOLUME

• ADMINISTRATION OF VASOCONSTRICTORS WILL IMPROVE PERIPHERAL
VASCULAR TONE, DECREASE VASCULAR CAPACITANCE, AND INCREASE VENOUS
RETURN, BUT SHOULD ONLY BE CONSIDERED ONCE HYPOVOLEMIA IS
EXCLUDED AS THE CAUSE OF THE HYPOTENSION AND THE DIAGNOSIS OF
NEUROGENIC SHOCK IS ESTABLISHED(DOPAMINE MAY BE USED FIRST).
 OBSTRUCTIVE SHOCK

• ALTHOUGH OBSTRUCTIVE SHOCK CAN BE CAUSED BY A NUMBER OF DIFFERENT

ETIOLOGIES THAT RESULT IN MECHANICAL OBSTRUCTION OF VENOUS RETURN.
• IN TRAUMA PATIENTS THIS IS MOST COMMONLY DUE TO THE PRESENCE OF
TENSION PNEUMOTHORAX. CARDIAC TAMPONADE OCCURS WHEN SUFFICIENT
FLUID HAS ACCUMULATED IN THE PERICARDIAL SAC TO OBSTRUCT BLOOD
FLOW TO THE VENTRICLES.