Obstetrics Simplified - Diaa M. EI-Mowafi

Shock in Obstetrics


Definition

Shock is a condition resulting from inability of the circulatory system to provide the tissues requirements from oxygen and nutrients and to remove metabolites.

Types and Causes

  • Haemorrhagic shock excessive blood loss may be due to:
    • Causes of bleeding early in pregnancy.
    • Causes of antepartum haemorrhage.
    • Causes of postpartum haemorrhage.
  • Neurogenic shock painful conditions my be due to:
    • Disturbed ectopic pregnancy.
    • Concealed accidental haemorrhage.
    • Forceps or breech extraction before full cervical dilatation.
    • Rough internal version.
    • Crédé’s method.
    • Rupture uterus.                
    • Acute inversion of the uterus.
    • Rapid evacuation of the uterine contents as in precipitate labour and rupture of membranes in polyhydramnios. This is accompanied by rapid accumulation of blood in the splanchnic area due to sudden relief of pressure (splanchnic shock).
  • Cardiogenic shock: ineffective contraction of the cardiac muscle due to
    • Myocardial infarction.         
    • Heart failure.
  • Endotoxic shock: generalised vascular disturbance due to release of toxins.
  • Anaphylactic shock: caused by sensitivity to drugs.
  • Other causes:
    • Embolism: amniotic fluid, air or thrombus.
    • Anaesthetic complications: as Mendelson's syndrome.
    • The shock may be caused by more than one factor as:
    • Incomplete abortion: leads to haemorrhagic and endotoxic shock.
    • Disturbed ectopic and rupture uterus: lead to haemorrhagic and neurogenic shock.

Classic Clinical Picture of Shock

  • Low blood pressure.
  • Rapid weak (thready) pulse. 
  • Pallor.
  • Cold clammy sweat.
  • Cyanosis of the fingers.
  • Air hunger.  
  • Dimness of vision.
  • Restlessness.
  • Oliguria or anuria.

HAEMORRHAGIC SHOCK

Classification of Haemorrhage

Class

Blood Loss%

Clinical Picture

I

15%

Normal pulse & blood pressure.
Tilt test +ve .

II

20-25%

Tachycardia.
Tachypnoea.
Pulse pressure (<30mmHg).
Low systolic pressure.
Delayed capillary filling.

III

30-35%

Skin: cold, clammy and pale.
Severe drop in blood pressure.
Restlessness.
Oliguria (<30 ml/hour).
Metabolic acidosis (blood pH <7.5).

IV

40-45%

Profound hypotension.
The carotid pulse is the only felt one.
Irreversible shock.

Tilt test

  • It is done in patient with considerable bleeding but the blood pressure and/ or pulse rate are normal.
  • When this patient is in a sitting position, she develops hypotension and / or tachycardia.

Phases of Haemorrhagic Shock

The normal pregnant woman can withstand blood loss of 500 ml and even up to 1000 ml during delivery without obvious danger due to physiological cardiovascular and haematological adaptations during pregnancy.

Phase of compensation

  • Sympathetic stimulation: It is the initial response to blood loss leading to peripheral vasoconstriction to maintain blood supply to the vital organs.
  • Clinical picture: Pallor, tachycardia, tachypnoea.

Phase of decompensation

  • Blood loss exceeds 1000 ml in normal patient or less if other adverse factors are operating.
  • Clinical picture: is the classic clinical picture of shock (see before).
  • Adequate treatment at this phase improves the condition rapidly without residual adverse effects.

Phase of cellular damage and danger of death

  • Inadequately treated haemorrhagic shock results in prolonged tissue hypoxia and damage with the following effects:
  • Metabolic acidosis: due to anaerobic metabolism initiated after lack of oxygen.
  • Arteriolar dilatation: caused by accumulation of metabolites leading to pooling and stagnation of blood in the capillaries and leakage of fluid into the tissues.
  • Disseminated intravascular coagulation: caused by release of thromboplastin from the damaged tissues.
  • Cardiac failure: due to diminished coronary blood flow.
  • In this phase death is imminent, transfusion alone is inadequate and if recovery from acute phase occurs residual tissue damage as renal and/ or pituitary necrosis will occur.

Management

Urgent interference is indicated as follow:

  • Detect the cause and arrest haemorrhage.
  • Establish an airway and give oxygen by mask or endotracheal tube.
  • Elevate the legs to encourage return of blood from the limbs to the central circulation.
  • Two or more intravenous ways are established for blood, fluids and drugs infusion which should be given by IV route in shocked patient. If the veins are difficult to find a venous cut down or intrafemoral canulation is done.
  • Restoration of blood volume by:
    • Whole blood: cross-matched from the same group if not available group O-ve may be given as a life -saving.
    • Crystalloid solutions: as ringer lactate, normal saline or glucose 5%. They have a short half life in the circulation and excess amount may cause pulmonary oedema.
    • Colloid solutions: as dextran 40 or 70, plasma protein fraction or fresh frozen plasma.
  • Drug therapy:
    • Analgesics: 10-15 mg morphine IV if there is pain, tissue damage or irritability.
    • Corticosteroids: Hydrocortisone 1gm or dexamethasone 20 mg slowly IV. Its mode of action is controversial; it may decrease peripheral resistance and potentiate cardiac response so it improves tissue perfusion.
    • Sodium bicarbonate: 100 mEq IV if metabolic acidosis is demonstrated.
    • Vasopressors: to increase the blood pressure so maintain renal perfusion.
      • Dopamine: 2.5m g/ kg/ minute IV is the drug of choice.
      • ß -adrenergic stimulant: isoprenaline 1mg in 500 ml 5% glucose slowly IV infusion.
  • Monitoring:
    • Central venous pressure (CVP): normal 10-12 cm water.
    • Pulse rate.              
    • Blood pressure.
    • Urine output: normal 60 ml/hour.
    • pulmonary capillary wedge pressure: Normal 6-18 Torr.
    • Clinical improvement in the: pallor, cyanosis, air hunger, sweating and consciousness.

Complications

  • Acute renal failure.
  • Pituitary necrosis (Sheehan’s syndrome).
  • Disseminated intravascular coagulation.

ENDOTOXIC (SEPTIC OR BACTERAEMIC) SHOCK

Obstetric Causes

  • 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, proteus, pseudomonas and bacteroids. The endotoxin is a phospholipopolysaccharide released by lysis of its cell envelope.
  • A similar picture is produced from exotoxin of ß-haemolytic streptococci, anaerobic streptococci and clostridia.

Pathology

Release of endotoxin results in increased lysosomal permeability and cytotoxicity. The sequence of events thereafter may occur in few minutes and include:

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 disseminated intravascular coagulation due to sudden massive plasmin generation with which the antiplasmins cannot cope.

Clinical Features

Endotoxic shock passes with 2 main stages:

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,
    • mottled cyanosis,   
    • purpura,
    • jaundice,
    • progressive mental confusion,
    • coma.

Irreversible stage

Prolonged cellular hypoxia leads to:

  • metabolic acidosis,
  • acute renal failure,   
  • cardiac failure,
  • pulmonary oedema,   
  • adrenal failure and ultimately death.

Differential Diagnosis

  • Amniotic fluid embolism.
  • Pulmonary embolism.  
  • Pulmonary aspiration syndrome.
  • Myocardial infarction.         
  • Incompatible blood transfusion.

Management

It includes 3 major lines of treatment:

Restoration of circulatory function and oxygenation

  • Replacement of blood loss: by whole blood, if not available start with colloids or crystalloids. The CVP measurement is essential to guard against circulatory overload.
  • Corticosteroids: as;
    • Hydrocortisone 1gm IV / 6 hours or,
    • Dexamethasone 20 mg initially followed by 200 mg/day by IV infusion.
  • β-adrenergic stimulants: as isoprenaline cause arteriolar dilatation, increase heart rate and stroke volume improving tissue perfusion. Blood volume must be normal prior to its administration.
  • Oxygen: if respiratory function is impaired.
  • Aminophylline: improves respiratory function by alleviating bronchospasm.

Eradication of infection

Antibiotic therapy:

  • Swabs for culture and sensitivity are taken first.
  • Antibiotic therapy is starting immediately till the result of culture and given by IV route. The therapy should cover the wide range of organisms:
 

Antibiotic

Acts upon

Dose

Regimen 1

Ampicillin or Cephalosporines

Aerobic gram+ organisms and gram- cocci.

500-1000 mg/6 hours.

 

Gentamycin

Aerobic gram- bacilli.

80 mg/ 8 hours.
(not to be given in the solutions).

 

Metronidazole

Anaerobic.

500 mg/ 8 hours.

Regimen 2

Clindamycin

Aerobic gram + organisms + gram- cocci + anaerobic organisms.

600 mg/ 6 hours.

 

Gentamycin

Aerobic gram- bacilli.

80 mg/ 8 hours.

Surgical treatment:

is indicated when there is retained infected tissues as in septic abortion. It should be removed as soon as antibiotic therapy and resuscitative measures have been started by:

  • suction evacuation,
  • digital evacuation, or
  • hysterectomy in advanced infection with a gangrenous (clostridium welchii) or traumatised uterus.

Correction of fluid and electrolyte deficits

Disseminated intravascular coagulation

Heparin therapy (see DIC) except if there is active bleeding where the condition is best treated by fresh blood transfusion.

AMNIOTIC FLUID EMBOLISM

Definition

Passage of amniotic fluid into the maternal circulation leads to sudden collapse during labour but can only be confirmed at necropsy.

Pathology

The condition is more common with strong uterine contraction, whether spontaneous or induced, occurs after rupture of membranes particularly when there are open maternal blood vessels in the placental site or in cervical lacerations.

The embolism passes to the pulmonary vessels leads to:

  • sudden death,
  • shock, or
  • Later death due to DIC and postpartum haemorrhage.

Clinical Picture

  • The onset is acute with sudden collapse, cyanosis and severe dyspnoea.
  • This is soon followed by twitching, convulsions and right side heart failure, with tachycardia, pulmonary oedema and blood stained frothy sputum.
  • If death does not occur in this stage, DIC develops within 1 hour leading to generalised bleeding.

Investigations

  • ECG: evidence of right side heart failure.
  • X-ray: non-specific mottled chest appearance.
  • Lung scan: with technetium-99m albumin shows perfusion defect.
  • Laboratory tests: evidence of DIC.

Differential Diagnosis

  • Acute pulmonary oedema.
  • Pulmonary aspiration (Mendelson’s) syndrome.
  • Other coagulation defects.

Treatment

Urgent treatment includes:

  • Oxygen: endotracheal intubation and positive pressure respiration is usually indicated as the patient is often unconscious.
  • Aminophylline: 0.5 gm slowly IV to reduce bronchospasm.
  • Isoprenaline:0.1gm IV to improve pulmonary blood flow and cardiac activity.
  • Digoxin and atropine: if central venous pressure is raised and pulmonary secretions are excessive.
  • Hydrocortisone: 1 gm IV followed by slow IV infusion causes vasodilatation and improves tissue perfusion.
  • Bicarbonate solution: if there is respiratory acidosis.
  • Low molecular weight dextran: reduces platelets aggregation in vital organs.
  • Heparin: for treatment of DIC if there is no active bleeding.
  • Vaginal delivery: is safer than C.S. if the baby is not yet delivered.

CARDIAC ARREST

Definition

Sudden circulatory collapse caused by sudden failure of the heart to pump the blood adequately.

Types

  • Complete cessation of mechanical and electrical activity: asystole.
  • Rapid ineffective activity: ventricular tachycardia and ventricular fibrillation.
  • Slow ineffective activity: sinus bradycardia and complete heart block.

In practice, asystole and ventricular fibrillation account for almost all cases of cardiac arrest.

Causes

Any cause of obstetric shock can end by cardiac arrest, the commonest of which are:

  • Severe haemorrhage.
  • Hypoxia due to eclampsia or anaesthesia.
  • Mendelson’s syndrome: gastric aspiration with pneumonitis.
  • Embolism of whatever the nature.

Diagnosis

  • Sudden collapse.  
  • Loss of consciousness.
  • Absence of pulse including the carotid and femoral pulse.
  • Apnoea and cyanosis of variable degree.
  • Fixed dilatation of the pupils.

N.B. Attempts to auscultate the heart, to record blood pressure or ECG are only time wasting procedures unless the patient is already being monitored during surgery.

Management

  • Urgent pairs of hands are needed to save the patient’s life.
  • Put the patient in the dorsal position onto a firm surface, even the floor.
  • A single firm thump with the closed fist over the lower sternum may be sufficient to correct the condition otherwise,
  • The following ABC steps are carried out:
    • Airway:
      • Clear it: from vomitus, blood, teeth, foreign body ...etc.
      • Maintain it: Pull mandible and tongue forward.
      • Insert an airway.
      • Endotracheal intubation as soon as possible.
    • Breathing:
      • One of the following is used:
      • Mouth-to-mouth artificial respiration.
      • Mask and ambubag with 100 % oxygen.
      • Cuffed endotracheal tube with intermittent positive pressure of 100% oxygen.
    • Cardiac massage:
      • Using the heel of one hand, with the other on top, and with the arms extended, apply pressure to the lower sternum using the full body weight.
      • This should provide a palpable femoral or carotid pulse.
      • The optimal compressions is 60 / minute in a ratio of 4:1 to ventillation.
    • Drip and Drugs:
      • Sodium bicarbonate 8.4% solution: to counteract metabolic acidosis. Give 100 ml initially and a further 10 ml for each subsequent minute of inadequate circulation.
      • Cardiac stimulants (inotropic drugs): can be given IV or intracardiac e.g.
        • Adrenaline 0.5-1.0 mg.      
        • Atropine 0.6 mg.
        • Isoprenaline 4 mg in 500 ml solution.
        • Dopamine 500 mg in 500 ml solution (1-3 m g/ kg/ min).
        • Calcium chloride 10% solution.
    • Electrocardiogram:
      • to assess the condition and response to the therapy.
    • Fibrillation treatment
      • Direct current (DC) defibrillator is used.

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Edited by Aldo Campana,