Obstetrical Shock Anupama Tamrakar Lecturer YNC Definition of

Obstetrical Shock Anupama Tamrakar Lecturer, YNC

Definition of Shock • A state in which capillary perfusion is inadequate to sustain life ----> Death of vital cells. • A state of circulatory inadequacy with poor tissue perfusion resulting in generalized cellular hypoxia.

Shock - Pathophysiology • Primary pathophysiologic mechanism in shock is impaired oxygen utilization by tissue • Impaired utilization encompasses a continuum • Impaired utilization may be from: • – reduced perfusion • – deficient uptake • – abnormal relative perfusion

• Shock represents one extreme of a continuum of SYSTEMIC INFLAMMATORY • RESPONSE SYNDROME (SIRS) characterized by (any 2): • – Fever or hypothermia • – Pulse > 90/ min • – Tachypnea (> 20/min or Pa. CO 2 < 32 torr • – Leukocytosis (> 12 K), Relative Leukopenia (<4 K), or > 10% immature forms

Types and Aetiology 1. Hypovolaemic • Haemorrhagic: APH, PPH, operative • Plasma loss: intestinal obstruction, acute pancreatitis • Dehydration: hyperemesis 2. Normovolaemic • Toxic: sepsis, anaphylaxis • Neurogenic: vasovagal, emotional, spinal anaesthesia • Metabolic: adrenal failure, acidosis, hypoxia • Cadiogenic: pulmonary embolism, MI, etc.

CAUSES OF HEMORRHAGIC SHOCK • Antenatal Ruptured ectopic preg, Incomplete abortion, MTP, Ut perforation during evacuation , APH, Ut rupture, Abdominal wall hematoma, Non obstetrical intra abdominal bleeding. • Intra natal uterine rupture. • Post natal PPH, Retained tissue , Thrombosis, Acute uterine inversion. Nonhaemorrhagic hypovolaemic shock , Burns Hyperemesis gravidarum , Ac. Diarrhoea

Haemorrhagic Shock • Associated with the postpartum or postabortal hemorrhage, ectopic pregnancy, placenta praevia, abruptio placenta, rupture of the uterus and obstetric surgery

Clinical Manifestations • Endotoxic shock passes with 2 main stages: 1. Reversible stage • It has 2 phases: • Early (warm) phase: there are; – hypotension, – tachycardia, – pyrexia, rigors, – flushed skin, – patient is alert, – leucocytosis develops within hours.

• Late (cold) phase: there are; – cold and clammy skin, – cyanosis, purpura, – jaundice, – progressive mental confusion, – coma.

2. Irreversible stage • Prolonged cellular hypoxia leads to: • metabolic acidosis, • acute renal failure, • cardiac failure, • pulmonary oedema, • adrenal failure and ultimately death.

Phases of Haemorrhagic Shock 1. Early phase (Compensatory Phase) 2. Intermediate phase (Reversible phase) 3. Late stage (Irreversible phase)

1. Compensatory Phase: mild vasoconstriction and with compensatory mechanism, relatively normal BP, tachycardia and diaphoresis, warm extremities, restless and anxious. 2. Reversible phase: hypotension, intense vasoconstriction leading to pale, tachycardia, cold periphery and sweating. Due to diversion of blood to vital organs, the pt remains conscious and the urine output is within normal limits. Still with adequate management, the shock state can be reversed.

Irreversible Phase • Continue hypotension and can not be reversed by replacement of fluid because of stagnation of blood at the micro vascular level • Cold and clammy extremities and skin will be ashen grey color • Metabolic acidosis • Coagulopathy and thrombocytopenia • Low volume pulse, oliguria, mental confusion

Management Principle of Management: • Stop bleeding • Replace the volume which has been lost

Management • Infusion and transfusion • Maintenance of cardiac efficiency and haemodynamic monitoring • Administraction of Oxygen by face mask at a rate of 6 – 8 l to avoid metabolic acidosis • Pharmacologic agents: Vasopressor • Control of haemorrhage • Monitoring vital signs, I/O, CVP, blood gas, etc

SEPTIC SHOCK ØNomenclatures - 1 Systemic inflammatory response syndrome (SIRS) is recognized by presence of one or two of the following : - i) temp <36 , or >38 degree centigrade. ii) HR >90 per minute. iii) blood gas Pa. CO 2< 4. 3 KPa (32 mm. Hg). iv) WBC >12000/mm 3 or with immature neutrophils. 2 Sepsis SIRS with clinical evidence of infection.

SEPTIC SHOCK ØNomenclature 3 Septic shock Sepsis with hypotension despite adequate fluid resuscitation. To diagnose it: - (i)Evidence of infection. (ii) +ve blood culture (iii) refractory hypotension , patient requiring vasopressors /inotropic drugs. 4 Sepsis with multi organ failure(MODS) Hypotension , hypoxia , oliguria metabolic acidosis , thrombocytopenia , DIC , decreased level of consciousness

Obstetrical Causes for Septic Shock • • Septic abortion. Prolonged rupture of membranes. Manipulations and instrumentations. Trauma. Retained placental tissues. Puerperal sepsis. Severe acute pyelonephritis.

Causative Organisms • Gram-negative bacilli: E. coli, pseudomonas and bacteroids. proteus, • exotoxin of ß-haemolytic streptococci, anaerobic streptococci and clostridia.

PREDISPOSING FACTORS IN OBSTETRICS TO SEPTIC SHOCK Post LSCS Endometritis(15 -85%) PROM Infected RPOC(1 -2%) Post vaginal delivery endometritis (1 -4%) Chorioamnionitis Water birth delivery - due to faecal contamination. Pyelonephritis , pneumonia , appendicitis. Toxic shock syndrome <1% Septic abortion RPOC , Uterine perforation peritonitis. • Pregnancy with retained IUCD. • Cx circlage in PROM cases. • Intra amniotic infection. • • •

Pathophysiology • Release of endotoxin results in increased lysosomal permeability and cytotoxicity. This leads to: • Stimulation of the adrenal medulla and sympathetic nervous system → constriction of arterioles and venules → local acidosis → arteriolar dilatation but with continuing constriction of the venules → capillary pooling of blood → haemorrhagic engorgement of bowel, liver, kidneys and lungs. • There is associated extensive DIC due to sudden massive plasmin generation with which the antiplasmins cannot cope.

SEPTIC SHOCK - SYMPTOMS � � Abdominal pain. Vomiting. Diarrhea. Fever — later on hypothermia

SEPTIC SHOCK MANAGEMENT • General--It includes initial management of shock and circulatory management which requires rapid blood volume expansion to correct the absolute and relative hypovolaemia and maintain end organ perfusion. • Improvement in maternal haemodynamic stability has direct effect on fetal viability. • LSCS for fetal distress in unstable mother will drive last nail in her coffin. • If fetal component is source of sepsis , then delivery becomes the essential part of active management.

SEPTIC SHOCK SPECIAL ASPECTS MANAGEMENT • Quickly transfer to tertiary medical institution. • Direct arterial and central venous monitoring. • Take samples for culture - blood , wound , higher swab from vagina and uterus , amniotic fluid , peritoneum , pouch of Douglas. • Intra venous broad spectrum antibiotics against gram +ve & gram -ve and anaerobes. • Removal of infective tissue : evacuation of uterus , colpotomy , laparotomy and if required caesarean hysterectomy. • Goal related therapy.

ADVANCES IN SEPSIS MANAGEMENT • Early goal – directed therapy - modifying the initial Rx to achieve mean arterial pressure >65 mm. Hg , urine out put >0. 5 ml/Kg/hr , CVP 8 -12 mm Hg and normal mixed venous oxygen saturation. An effort to reduce end organ damage and tissue death. It improves outcome in septic patients. • Insulin therapy - aggressive control of blood sugar has been demonstrated to improve outcome in septic patients. • Activated protein C (APC) - Patient with sepsis has decreased APC levels. Its administration decreases mortality and reduces organ dysfunction.

ADVANCES IN SEPSIS MANAGEMENT • Corticosteroid therapy ? -- In un selected septic paient it may worsen outcome because of secondary infection. • In critically ill patient there may be relative adrenal insufficiency. In septic shock /the affected adrenals may not respond to increased demand of adrenocorticosteroids. Studies on Cortisone therapy in septic shock , have different results. Its beneficial effects in obstetrical sepsis is unknown.