Shock in Obstetrics

OBSTETRIC SHOCK

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

1-Haemorrhagic shock
excessive blood loss may be due to:
bleeding early in pregnancy.
antepartum haemorrhage.
postpartum haemorrhage.

2-Neurogenic shock

painful conditions my be due to:
1. ectopic pregnancy.
2.Concealed accidental haemorrhage.
3.Forceps or breech extraction before full cervical dilatation.
4.Rough internal version.
5.Rupture uterus.
6.Acute inversion of the uterus.
7.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).


3-Cardiogenic shock
ineffective contraction of the cardiac muscle due to
1.Myocardial infarction.
2.Heart failure.

4-endotoxic shock

generalised vascular disturbance due to release of toxins.
5-anaphylactic shock
caused by sensitivity to drugs.

6-others

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.

clinical presentation

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

• Clinical Picture

• Blood Loss%
• Class
• Normal pulse & blood pressure.Tilt test +ve .
• %15
• I
• Tachycardia.Tachypnoea. Pulse pressure (<30mmHg).Low systolic pressure. Delayed capillary filling.
• %20-25
• II
• Skin: cold, clammy and pale.Severe drop in blood pressure. Restlessness.Oliguria (<30 ml/hour).Metabolic acidosis (blood pH <7.5).
• -%30-35
• III
• Profound hypotension.The carotid pulse is the only felt one. Irreversible shock.
• -%40-45
• IV

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.


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.
STAGES OF HAEMORRHAGIC SHOCK

Stage 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.

Stage 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.

stage of cellular damage&danger of death

Inadequately treated haemorrhagic shock results in prolonged tissue hypoxia and damage with the following effects:
• Metabolic acidosis
• Arteriolar dilatation
• Disseminated intravascular coagulation
• Cardiac failure
• 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
• 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 coagulation screen,blood group&cross match.thereafter 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.
• Detect the cause&arrest bleeding

Restoration of blood volume by:

• 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
• Whole blood: cross-matched from the same group if not available group O-ve may be given as a life -saving.

drugs

• 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.
• Clinical improvement in the: pallor, cyanosis, air hunger, sweating and consciousness


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

ENDOTOXIC SHOCK(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.

clinical presentation

A-Reversible stage
It has 2 phases:
1-Early (warm) phase:
hypotension,
tachycardia,
pyrexia,
rigors,
flushed skin,
patient is alert,
leucocytosis develops within hours.
2-Late (cold) phase:
cold and clammy skin,
mottled cyanosis,
purpura,
jaundice,
progressive mental confusion,
coma.


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

management

1-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.

2-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:


• Dose
• Acts upon
• Antibiotic
• 500-1000 mg/6 hours.
• Aerobic gram+ organisms and gram- cocci.
• Ampicillin or Cephalosporines
• Regimen 1
• 80 mg/ 8 hours.(not to be given in the solutions).
• Aerobic gram- bacilli.
• Gentamycin
• 500 mg/ 8 hours.
• Anaerobic.
• Metronidazole
• 600 mg/ 6 hours.
• Aerobic gram + organisms + gram- cocci + anaerobic organisms.
• Clindamycin
• Regimen 2
• 80 mg/ 8 hours.
• Aerobic gram- bacilli.
• Gentamycin


3-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.

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 presentation

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.

Urgent treatment

• Oxygen: endotracheal intubation and positive pressure respiration is usually indicated as the patient is often unconscious.
• Aminophylline
• Isoprenaline
• Digoxin and atropine
• Hydrocortisone

Bicarbonate solution

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.


Coagulation disorders

• Normal hemostasis: requires 3 main factors:

• Vascular constriction
• Platelet aggregation and formation of platelet plug
• Fibrin formation through the coagulation system
• When these factors stop bleeding, the fibrinolytic system start to remove the thrombus and restore the vascular patency

• Coagulation system during pregnancy:

• Pregnancy represent a hypercoagulable state. This include the following:
• Plasma fibrinogen concentration rises during pregnancy by about 50%.
• Increase in factors V, VII, VIII, IX, X, XII.

Venous thromboembolism(TE)

is the most common cause of maternal death during pregnancy.It also causes significant morbidity by the postphlebitic syndrome
The incidence of thromboembolic complications, pulmonary thromboembolism and deep vein thrombosis presented during pregnancy is around 1 in 1000 with a further 2 per 1000 women presenting in the puerperium.

• Risk factors:

• A-factors related to pregnancy
• Hypercoagulable state of pregnancy.
• Decrease activity of naturally occurring anticoagulant.
• Decrease fibrinolytic activity.
• Increase tendency to venous stasis during pregnancy.
• Operative delivery ,increasing Age and parity, ,Obesity ,restricted activity: HT, DM, PP, multiple pregnancy, heart disease (bed rest).


• B:factors not related to pregnancy
• Previous TE.
• Lupus anticoagulants, anticardiolipin antibodies, and antiphospholipid syndrome.
• Inherited thrombophilia like antithrombin III deficiency, protein C deficiency, protein S deficiency.
• smoking

Clinical Features of Venous TE:

Superficial thrombophlebitis:
This means inflammation of a superficial vein which if extended to a deep vein it carries a risk of PE. Active mobilization of the affected limb is encouraged to prevent DVT.

2. Deep Vein Thrombosis (DVT) :

The classical signs of DVT are leg edema, calf tenderness,
and positive Homans sign, which is calf pain on dorsiflexion of the foot,
it could be asymptomatic.

3-pulmonary embolism(PE):

a. Massive PE: cyanosis, shortness of breath, chest pain, hemoptysis.
b. Small PE: transient dyspnea, tinge of cyanosis, some pleuritic chest pain, unproductive cough, unexplained pyrexia, tachycardia, leukocytosis.


• DIGNOSIS
• Clinical features usually affects left femoral vein.
• Investigations
• Impedance plethysmography (IPG)
Dopplar US
Contrast venography, gold standard.
Iodine 125 fibrinogen
Radiological studies are contraindicated in pregnancy

Management of venouthromboembolism

Acute phase treatment.
Chronic phase treatment.

Acute phase treatment:

• Thrombolytic therapy:
• by streptokinase, and tissue plasminogen activaters.
2. Anticoagulants: unfractionated heparin 40,000 IU daily continuous intravenous infusion
Heparin is given for 3-7 days.
Low molecular weight heparin has replaced unfractionated heparin.
3. Surgery


Chronic phase treatment:
Warfarin which crosses the placenta.
Side effects : during pregnancy is teratogenicity and bleeding tendency in the fetus, bleeding in the mother.
Reversal of the effect is by stopping the drug, it will take three days to reserve the action, so we can give FFP and vitamin K.

Disseminated intravascular coagulationDIC

trigger mechanism of DIC during pregnancy:
Endothelial injury:
preeclampsia.
Hypovolemia.
septicemia

• 2. Release of thromboplastin as in:

• Abruptio placentae.
• Amniotic fluid embolism.
• Retained dead fetus.
• Intrauterine sepsis
• Hydatidiform mole
• Placenta accreta

• 3. Release of phospholipid as in:

• Intravascular hemolysis
• Incompatible blood transfusion
• Large fetomaternal bleed
• septicemia


• Clinical manifestation of DIC:
• Asymptomatic: compensated state. There is lab evidence of increased production and breakdown of coagulation factors, as in PET and in retained dead fetus.

2. Variable degrees of thrombocytopenia as in small abruptio placentae and in severe PET.

3. Massive uncontrollable hemorrhage as abruptio placentae, amniotic fluid embolism and eclampsia.

• Management:

• Fluid replacement to avoid renal shut down usually by simple crystalloid eg Hartmanns solution 2-3 times the estimated volume blood loss.
• FFP which contains all coagulation factors
• Fresh blood transfusion