Claire Roberts rvn dipavn(Surg) vncertecc aetiology and Patient Presentation of the gdv patient

Hypotension

Shock is very common in GDV patients, low blood pressure is caused by the dilated stomach compressing the vena cava and reducing blood flow back to the heart, this reduces the subsequent cardiac output. Patients can be hypovolaemic as well due to fluid sequestration. Septic shock can develop later, especially if stomach necrosis has occurred.

Hypotension means that perfusion of vital organs is compromised and oxygen delivery is not adequate. In this situation the tissues become hypoxic and revert to an anaerobic energy production. A by-product of this energy production is lactic acid. This is lactic acidosis.

Measuring lactate can help to predict the outcome of GDV cases. 99% of GDV patients with a lactate <6mmol/l are likely to survive compared to 58% who had a lactate >6mmol/l.

It is vital to reverse this chain of events and prevent lactate from building up.

This is achieved with fluid therapy and stomach decompression. Hartman's is the fluid of choice, it is isotonic and contains precursors of bicarbonate to counteract acidosis whereas saline although isotonic can be acidifying which is not helpful in an acidotic patient! Fluid boluses of 10-20ml/kg over 15 minutes can be given to improve blood pressure. Careful assessment of cardiovascular status should take place after each bolus e.g. BP and HR. A continuous infusion of 10ml/kg/hr should be provided throughout anaesthesia to compensate for vasodilation produced by anaesthetic drugs.

Colloids are not currently recommended for critical patients unless there has been acute haemorrhage. However if the patient has a low PCV or haemoglobin level, then oxyglobin could be considered to improve oxygen carrying ability and to provide some oncotic support.

Hypertonic saline can be considered for a severely hypotensive patient. 7.2% Saline can be given as a bolus of 4ml/kg. Hypertonic saline draws fluid from the intracellular space into the intravascular space increasing circulating volume. It must be followed by crystalloids to replace the fluid taken from the intracellular space.

Once the stomach has been untwisted there is a risk that endotoxins and cytokines will be released due to the restoration of perfusion to compromised areas of tissue. These can cause a reduction in myocardial contractility and vasodilation. This is a particular risk if the stomach wall has become necrotic. The release of cytokines can induce systemic inflammatory response (SIRS).

Positive inotropes can be used to improve blood pressure (once any fluid deficits have been corrected). They can either improve contractility or improve systemic vascular resistance (vasodilation).

The two most common positive inotropes are Dobutamine and Dopamine. Dobutamine increase myocardial contractility which will increase cardiac output and blood pressure. Dopamine increase contractility but at high doses it will also increase systemic vascular resistance. Both drugs can cause hypertension, tachycardia and arrhythmias so there must be blood pressure and continuous ECG monitoring available to detect these problems.