SHOCK IN OBSTETRICS

SHOCK IN OBSTETRICS

DEFINITION

A state of circulatory impairment characterized by defective tissue perfusion resulting in abnormal cellular function and metabolism. This leads to a clinical syndrome of signs of decreased perfusion of vital organs, with possible alterations in the mental status (somnolence) and oliguria (urine output <30 ml/Hr.)

Types and etiology of shock

1. Hypovolaemic shock: secondary to– Bleeding (various causes of bleeding in early pregnancy, ante- or

postpartum hemorrhage).– Other causes of fluid loss (e.g. nasogastric suction or diarrhea).

2. Distributive shock: secondary to increased venous pooling (i.e. early septic shock, peritonitis, anaphylaxis and neurogenic shock).

3. Cardiogenic shock: secondary to decreased myocardial contractility and function (as in myocardial infarction).

4. Obstructive shock: secondary to mechanical obstruction (i.e. cardiac tamponade, massive pulmonary embolism or thrombosed prosthetic valve).

CLINICAL PICTURE

Hypotension ( a BP decrease of 50-60 mmHg or BP <100 mmHg) & subnormal temperature.

Tachypnia & tachycardia (weak rapid -thready- pulse).

Pallor, cyanosis of fingers and cold clammy sweat. Dimness of vision and mental confusion. Oliguria.

Remote Complications

Renal failure (due to cortical necrosis). Postpartum anterior pituitary necrosis

(Sheehan syndrome).

HYPOVOLEMIC OR HEMORRHAGIC SHOCK

A healthy pregnant woman can lose 25% of her blood volume (1500ml) before clinical signs of shock are evident. However, the conditions that predispose to the development of shock in obstetrics include: a) anemia & malnutrition; b) bleeding in early pregnancy, antepartum or postpartum hemorrhage; c) prolonged labor with dehydration and acidosis; d) hypertensive with pregnancy.

Compensatory Mechanisms Arterioles: they control capillary blood flow in various organs. They‘re

resistance vessels controlled by the CNS. Venules: they contain 70% of the total blood volume. They‘re passive

resistance vessels controlled by humoral factors. Catecholamine release during hemorrhage causes increased venular

tone resulting in autotransfusion from this capacitance reservoir. There is compensatory increase in heart rate, systemic and pulmonary

vascular resistance, and myocardial contractility. There is redistribution of cardiac output & blood volume by selective

centrally mediated arteriolar constriction resulting in decreased blood flow to kidneys, splanchnic bed, uterus and skin with relative maintenance of blood flow to the heart, brain & adrenal glands (organs that autoregulate their own flow).

Decompensation When blood volume deficit exceeds 25%. Rapid clinical deterioration results from

maldistribution of blood flow that causes local tissue hypoxia & metabolic acidosis, producing a vicious circle of vasoconstriction, organ ischemia and cellular death.

Loss of capillary membrane integrity. Increased platelet aggregation resulting in small

vessel occlusion. Electrolyte shifts: Na+ & H2O enter skeletal muscles

and cellular K+ is lost to the extracelluar space.

Classification Of Shock Based On Extent Of Blood Loss

Parameter Class I Class II Class III Class IV

Blood volume lost (%) <15 15-30 30-40 >40

Pulse rate (beats/min) <100 >100 >120 >140

Supine blood pressure Normal Normal Decreased Decreased

Urine output (ml/hr) >30 20-30 5-15 <5

Mental status Anxious Agitated Confused Lethargic

Pathophysiology

System Effect

CNS Cerebral Confusion, somnolence, coma and combativeness

Hypothalamus Fever, hypothermia

CVS BP Hypotension (vasodilatation)

Cardiac Increased cardiac output (early), myocardial depression (late), tachyarrhythmia

Pulmonary Shunting with hypoxemia, diffuse infiltrates (capillary leak)

Renal Hypoperfusion (oliguria), acute tubular necrosis

Hematological Thrombocytopenia, leukocytosis, DIC

TREATMENT General measures: Adequate ventilation providing oxygen by mask, nasal tube or

tracheal intubation if needed. Insertion of two wide bore cannulas with blood sample

collection for blood grouping, Rh & cross-matching, CBC, electrolytes, liver & kidney function tests, blood sugar and coagulation profile (PT, PTT, fibrinogen & FDPs).

Warmth, recumbent position with legs slightly elevated. Morphine to alleviate pain and apprehension if needed.

TREATMENTFluid, blood and blood component replacement:1. Crystalloid solutions as lactated Ringer’s solution or normal

saline (basic therapy for acute hemorrhage is crystalloid and blood).

2. Colloid therapy (as plasma substitutes) will provide more volume expansion than crystalloids.

3. Whole blood: only used in torrential bleeding.4. Packed RBCs are usually used.

Blood component replacement is rarely necessary with acute component replacement of 5-10 packed RBCs or less. Transfusion is needed when Hb concentration falls to <8 g/dL or Ht <25 %.

5. Red cell substitutes: still under research.

Blood Components Commonly Transfused In Obstetrics

Product Indication content Effect

Whole blood (450 ml) Symptomatic anemia with large volume deficits

All components Increases Ht 3-4 % per unit

Packed RBCs (250 ml) Symptomatic anemia Erythrocytes Increases Ht 3-4 % per unit

Fresh frozen plasma (FFP 250 ml)

Deficit of labile and stable coagulation factors

All clotting factors Supplies fibrinogen 150 mg per unit and other factors

Cryoprecipitate (50 ml) Hypofibrinogenaemia Factors VIII, VWF, XIII, fibronectin, and fibrinogen

Supplies selected clotting factors

Platelets (50 ml) Bleeding from thrombocytopenia

Platelets Increases platelet count by 5000-8000/μl per unit

TREATMENT Monitoring: Vital signs, urine output, central venous

pressure (CVP), pulmonary artery pressure (by Swan-Ganz catheter in selected patients) & repeat lab investigations.

Vasoactive and inotropic agents:– Dopamine.– Dobutamine.– Epinephrine.– Norepinephrine.

SEPTICEMIC SHOCK

Etiology:

As pelvic infection is polymicrobial, septic shock may be caused most commonly by endo-toxin producing enterobacteriaceae family especially E. coli, less often by aerobic and anaerobic streptococci, Bacteroides and Clostridium species. Virulent exotoxin producing Group A ß-hemolytic streptococci and also Staphylococcus aureus may also be the cause.

PathophysiologyBacterial toxins result in mediator release with: Activation of complement, kinins and the coagulation system

causing DIC & induction of fibrinolytic state with bleeding. Selective vasodilatation with maldistribution of blood flow. Leukocyte & platelet aggregation causing capillary plugging. Vascular endothelial injury causing profound capillary leakage. Early septic shock is a form of distributive shock while in late

stages it is both distributive and cardiogenic. The end result of this cascade is septic shock syndrome with multiple organ failure.

CLINICAL PICTURE

Passes into 3 stages of increasing severity: systemic inflammatory response syndrome (SIRS), severe sepsis then septic shock.

TREATMENT

Aggressive fluid replacement. Oxygenation and ventilation.

Administration of vasopressor and inotropic agents.

Broad spectrum antibiotics. Removal of the infectious source. Steroids and NSAID: are not beneficial. Immunotherapy is still under research.

CARDIOGENIC SHOCK

Can also occur in the setting of septic shock or hemorrhagic shock, especially in patients who have baseline cardiovascular disease. Treatment requires invasive monitoring and dealing with the underlying disorder.

NEUROGENIC SHOCK

Etiology: trauma and tissue damage as in cases of: Disturbed extrauterine pregnancy. Concealed accidental hemorrhage. Difficult forceps delivery or breech extraction (especially if the cervix

isn’t fully dilated). Difficult internal version. Repeat rough attempts at Crede’s method. Rupture of the uterus or cervical tears extending into the lower uterine

segment. Acute inversion of the uterus. Rapid evacuation of the uterus as in precipitate labor and

polyhydramnios Retained placenta especially for more than 2 hours.

Differences between Neurogenic and Hemorrhagic Shock

Neurogenic shock Hemorrhagic shock

The patient is quiet and apathetic The patient is restless and anxious with air hunger

No external or internal bleeding External or internal bleeding

Superficial veins are full of blood Superficial veins are collapsed

Hemoconcentration Hemodilution

Slow pulse Weak and rapid pulse

Slow and shallow respiration Rapid and shallow respiration

TREATMENT

General measure: mentioned earlier. Fluid replacement. Vasopressor and inotropic agents. Dealing with the cause.