Descriptive study of differences in acute kidney injury progression patterns in General and Cardiac Intensive Care Units.

BACKGROUND: Acute kidney injury is common in critically ill patients with detrimental effects on mortality, length of stay and post-discharge outcomes. The Acute Kidney Injury Network developed guidelines based on urine output and serum creatinine to classify patients into stages of acute kidney injury. METHODS: In this analysis we utilize the Acute Kidney Injury Network guidelines to evaluate the acute kidney injury stage in patients admitted to general and cardiac intensive care units over a period of 18 months. Acute kidney injury stage was calculated in real time hourly based on the guidelines and using these temporal stage scores calculated for the population; the prevalence and progression of acute kidney injury stage was compared between the two units. We hypothesized that the prevalence and progression of acute kidney injury stage between the two units may be different. RESULTS: More cardiac intensive care unit patients had no acute kidney injury (stage <1) during their intensive care unit stay but more cardiac intensive care unit patients developed acute kidney injury (stage >1), compared to the General Intensive Care Unit. Both at intensive care unit admission and discharge, more General Intensive Care Unit patients had acute kidney injury; however, the number of cardiac intensive care unit patients with acute kidney injury was three times higher at discharge than admission. Acute kidney injury developed in a different pattern in the two intensive care units over five days of intensive care unit stay. In the General Intensive Care Unit, acute kidney injury was most prevalent on second day of intensive care unit stay and in cardiac intensive care unit acute kidney injury was most prevalent on the third day of intensive care unit stay. We observed the biggest increase in new acute kidney injury in the first day of General Intensive Care Unit and second day of the cardiac intensive care unit stay. CONCLUSIONS: The study demonstrates the different trends of acute kidney injury pattern in general and cardiac intensive care unit patient populations highlighting the earlier development of acute kidney injury on General Intensive Care Unit and more prevalence of acute kidney injury on discharge from cardiac intensive care unit.

Randomized controlled trial comparing the effect of 8.4% sodium bicarbonate and 5% sodium chloride on raised intracranial pressure after traumatic brain injury.

BACKGROUND: Hypertonic sodium chloride solutions are routinely used to control raised intracranial pressure (ICP) after traumatic brain injury but have the potential to cause a hyperchloremic metabolic acidosis. Sodium bicarbonate 8.4% has previously been shown to reduce ICP and we have therefore conducted a randomized controlled trial to compare these two solutions. METHODS: Patients with severe traumatic brain injury were randomly allocated to receive an equiosmolar dose of either 100 ml of sodium chloride 5% or 85 ml of sodium bicarbonate 8.4% for each episode of intracranial hypertension. ICP and blood pressure were measured continuously. Arterial pCO(2), sodium, chloride, osmolality, and pH were measured at intervals. RESULTS: We studied 20 episodes of intracranial hypertension in 11 patients. Treatments with 8.4% sodium bicarbonate and 5% sodium chloride reduced raised ICP effectively with a significant fall in ICP from baseline at all time points (P < 0.001). There was no significant difference in ICP with time between those episodes treated with 5% sodium chloride or 8.4% sodium bicarbonate, P = 0.504. Arterial pH was raised after treatment with 8.4% sodium bicarbonate. CONCLUSIONS: An equiosmolar infusion of 8.4% sodium bicarbonate is as effective as 5% sodium chloride for reduction of raised ICP after traumatic brain injury when infused over 30 min.

Sodium bicarbonate lowers intracranial pressure after traumatic brain injury.

BACKGROUND: Hypertonic saline is routinely used to treat rises in intracranial pressure (ICP) post-traumatic head injury. Repeated doses often cause a hyperchloremic metabolic acidosis. We investigated the efficacy of 8.4% sodium bicarbonate as an alternative method of lowering ICP without generating a metabolic acidosis. METHODS: We prospectively studied 10 episodes of unprovoked ICP rise in 7 patients treated with 85 ml of 8.4% sodium bicarbonate in place of our usual 100 ml 5% saline. We measured ICP and mean arterial pressure continuously for 6 h after infusion. Serum pH, pCO(2), [Na(+)], and [Cl(-)] were measured at baseline, 30 min, 60 min and then hourly for 6 h. RESULTS: At the completion of the infusion (t = 30 min), the mean ICP fell from 28.5 mmHg (+/-2.62) to 10.33 mmHg (+/-1.89), P < 0.01. Mean ICP remained below 20 mmHg at all time points for 6 h. Mean arterial pressure was unchanged leading to an increased cerebral perfusion pressure at all time points for 6 h post-infusion. pH was elevated from 7.45 +/- 0.05 at baseline to 7.50 +/- 0.05, P < 0.01 at t = 30 min, and remained elevated. Serum [Na(+)] increased from 145.4 +/- 6.02 to 147.1 +/- 6.3 mmol/l, P < 0.01 at t = 30 min. pCO(2) did not change. CONCLUSIONS: A single dose of 8.4% sodium bicarbonate is effective at treating rises in ICP for at least 6 h. Serum sodium was raised but without generation of a hyperchloremic metabolic acidosis.

Death from paracetamol overdose despite appropriate treatment with N-acetylcysteine.

A case of death from severe paracetamol poisoning which presented early and received appropriate treatment according to evidence-based guidelines is presented here. It is very rare for patients to die from paracetamol poisoning when they receive N-acetylcysteine (NAC) within 8 h of ingestion. The patient had a marked lactic acidosis on presentation to hospital. This case demonstrates that a patient can die from paracetamol poisoning despite early and appropriate treatment, and raises the question whether lactic acidosis in a patient following paracetamol overdose should prompt the initiation of NAC treatment while awaiting paracetamol levels.