Resistant Hypotension Research Articles

Circulatory support of the sick preterm infant

In the majority of preterm infants, especially during the immediate postnatal period, hypotension is primarily caused by abnormal peripheral vasoregulation and/or myocardial dysfunction and not by absolute hypovolemia. Therefore, aggressive volume resuscitation is not warranted and is potentially harmful. Volume support should be limited to 10–20ml/kg of isotonic saline administration and, if sustained normalization of the blood pressure cannot be achieved, early initiation of cardiovascular pharmacological support is recommended. However, in preterm infants who present with an identifiable volume loss, the kind of fluid lost should first be replaced. Due to its beneficial cardiovascular and renal actions, dopamine is the drug of choice in the treatment of neonatal hypotension. Dobutamine may be added if myocardial dysfunction persists or develops during dopamine treatment. In some critically ill preterm infants, escalation of dopamine therapy or addition of epinephrine is necessary yet not always effective indicating the development of pressor resistant hypotension. Downregulation of cardiovascular adrenergic receptors and some degree of adrenal insufficiency may explain this phenomenon. In these patients, a brief course of steroid treatment may be successful in stabilizing the cardiovascular status and decreasing the requirement for pressor/inotrope support. However, well-designed randomized and controlled clinical trials are needed in the future to determine the effectiveness and potential short- and long-term side effects of steroid administration in preterm infants with pressor-resistant hypotension. In summary, management of the critically ill hypotensive preterm infant remains challenging and requires a better understanding of the pathophysiology of neonatal shock and improvements in our ability to evaluate cardiac output, organ blood flow, and tissue perfusion at the bedside.

Hyperkalaemia in acute leukaemia: a sign of adrenocortical insufficiency.

To evaluate adrenal cortical reserve function in hyperkalaemic patients with acute leukaemia (AL). In hyperkalaemic AL patients, after basal blood collection for cortisol, rapid adrenocorticotropic hormone (ACTH) stimulation test was performed with human a1-24-ACTH 0.25 mg, intravenously. Sixty minutes following injection, additional plasma was obtained for cortisol. Normal response was a peak cortisol level greater than 15 micrograms dL-1 with an increment greater than 5 micrograms dL-1. Hacettepe University Hospital, Ankara, Turkey. Newly diagnosed AL patients with plasma K+ values exceeding 4.5 mmol L-1, who had never received antileukaemia therapy were eligible for entry into the trial. Thirteen patients fulfilled these criteria. Twenty AL patients with normal serum K+ levels were studied as controls. In six patients with hyperkalaemia, adrenal cortical response to rapid ACTH test was inadequate. One patient died during induction chemotherapy due to sepsis. Five of the remaining patients entered remission. Repeat ACTH tests during remission revealed normalization of the adrenocortical function in these patients. However, in only one patient with normal serum K+ level, adrenocortical reserve was decreased. We suggest that in any AL patient with hyperkalaemia, adrenal reserve function should be evaluated with rapid ACTH stimulation test. In states of resistant hypotension and hyperkalaemia, steroids may be life saving.

Octreotide controls resistant postural hypotension

Octreotide controls resistant postural hypotension