Haemorrhagic Shock, Disseminated Intravascular Coagulation and Obstetric Resuscitation

Definition

The simplest definition of shock is inadequate oxygen supply for cellular demand. Problems can exist at either the supply or demand end of this balance. In pregnancy, there is a higher metabolic requirement from the developing fetoplacental unit and maternal changes of pregnancy. Physiologic adaptations of the cardiovascular system normally provide an increase in cardiac output and red cell mass to facilitate oxygen delivery to meet this need. Complex pregnancies (e.g. multiples, those with significant medical comorbidities or sepsis) have a higher demand and are therefore more vulnerable to imbalance.

Incidence

The incidence of haemorrhagic shock is hard to define. Most definitions depend on the onset of hypotension, but this is a late sign in an obstetric population. It is generally accepted that life-threatening peripartum haemorrhage occurs in around 1 in 1000 maternities in the developed world.

Pathophysiology

With haemorrhage, the fundamental problem is supply-end failure of effective circulating volume and oxygen-carrying capacity of the blood. At cellular level, there is a transition from normal, aerobic metabolism to anaerobic processes. There is an accumulation of by-products of anaerobic metabolism (such as lactic acid) which is proportionate to the oxygen debt accruing and, ultimately, a risk of cell death.

At tissue level, exsanguinating haemorrhage can be severe enough to cause cardiac arrest. Complete lack of perfusion to brain and heart are irreversibly fatal within minutes of the onset of complete anoxia. More usually, the hypoperfusion resulting from reduced circulating volume and vasoconstriction (in an attempt to sustain blood pressure and prioritize blood flow to vital organs) results in progressive end-organ damage, relative to both degree and duration of haemorrhagic shock. End-organ damage exacerbates imbalance at the supply end in a cycle of amplification where:

• acute lung injury impairs oxygenation at the alveolar interface with downstream hypoxic effect

• acute renal impairment contributes to global acidosis and worsens haemostatic function, thereby increasing volume of haemorrhage

• liver hypoperfusion results in reduced synthetic function of endogenous clotting factors necessary to stem evolving coagulopathy

• myocardial ischaemia from hypotension and anaemia (and ergot alkaloids to treat uterine atony) decreases cardiac output and global perfusion.

Acute haemorrhage also provokes maladaptive changes in vascular endothelium that increase membrane permeability and cause fluid leak from the intravascular to extravascular space. This exacerbates the reduction in effective circulating volume and localized hypoxia within tissues. Dysregulated endothelium contributes to systemic coagulopathy and increases severe morbidity and mortality from the shock state.

Clinical Findings

Activation of a number of stress responses (catecholamine, endogenous corticosteroid, and renin-based systems) drives adaptation to acute blood loss. A classification of haemorrhagic shock illustrating typical clinical responses is adapted from the American College of Surgeons Committee on Trauma ( Table 29.1 ).

While a useful guide, classic responses to percentage of blood volume lost need to be considered in light of increased blood volume in pregnancy (up to 100 mL/kg versus 70 mL/kg for the nonpregnant state – variation in absolute body weight denotes large differences in percentage of circulating volume lost for a given volume), normal physiologic adaptations (these may overlap with ‘pathological’ states for heart rate especially) and hypotension, which is a late clinical sign in the obstetric population. A systematic review of the relationship between blood loss and clinical signs shows substantial variability in associations for traditional bedside indicators of heart rate and systolic blood pressure. However, clinical sign derivatives, in particular shock index (SI), seem to be a better indicator of severity of haemorrhage. The SI is calculated as heart rate divided by systolic blood pressure. A value above 0.9 (i.e. the heart rate is above systolic blood pressure) is an early indication of significant hypovolaemia and should trigger a treatment response.

Diagnosis

Early recognition of the physiological adaptations to acute haemorrhage ( Table 29.1 ) is key, and may be facilitated by use of early warning scoring (‘track and trigger’) systems to reveal worsening trends of abnormal vital signs. Identification of the source of haemorrhage directs treatment to ‘turn off the tap’ and limit hypovolaemia, hypoperfusion, oxygen debt and overall morbidity. Overt obstetric haemorrhage is easy to measure gravimetrically, and can help to categorize severity of haemorrhage early and thereby predict the nature and level of intervention required. Anticipation of covert obstetric haemorrhage needs to be judged in the setting of clinical signs. Bedside abdominal or transvaginal ultrasound can rapidly assess potential sites of concealed haemorrhage, and transthoracic echocardiography can be used to examine both cardiac filling and function in a matter of minutes. Advanced radiological assessment with either CT or MRI may be appropriate in certain circumstances (but should never delay resuscitative efforts). Other radiological modalities such as angiographic assessment offer the potential for diagnosis and treatment, as does exploratory laparotomy in certain, selected cases.

Laboratory testing is useful to try to define the degree of hypoperfusion and oxygen debt already present (pH, base excess and lactic acid/lactate level); the oxygen carrying capacity of blood (P o ₂ and Hb); coagulation status to establish ‘haemostatic competence’ and predict progression of haemorrhage and likely transfusion requirement (activated partial thromboplastin time [APTT], prothrombin time [PT], platelets and Clauss fibrinogen); electrolyte levels to guide replacement and maintain homeostasis of cardiac (potassium, calcium) and clotting function (calcium); and renal and liver indices to establish the presence of end-organ dysfunction resulting from the shock state. Whole blood viscoelastometric testing (thromboelastometry/thromboelastography) to assess coagulation may be available in some units. These are near-patient devices producing rapid diagnostic information on adequacy of haemostasis, and they assess both clot formation and lysis.

Whatever diagnostic modalities are used, repeat assessment at time intervals proportionate to the severity of haemorrhage and shock is important to guide initial management and evaluate response to ongoing therapy. Management of haemorrhagic shock is complementary to that of haemostatic failure in DIC so both are discussed in tandem below (see later: Management).