Category Archives: ICU

Stuff relevant to patients on ICU

Sodium lactate for raised ICP

Lactate may be an important metabolic substrate for injured brain and sodium lactate may have beneficial effects on cerebral oedema and cerebral blood flow. Sodium lactate was compared with 20% mannitol in severely brain injured patients with cranial hypertension in a randomised controlled trial. Sodium lactate was more likely to lower ICP, and to have a sustained effect on ICP. A nonsignificant improvement in one year outcome was seen with sodium lactate, although the study was not powered for this endpoint. These promising findings should prompt a larger multicentre study.

Sodium lactate versus mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients
Intensive Care Med. 2009 Mar;35(3):471-9

Is defib danger overstated

No rescuer or bystander has ever been seriously harmed by receiving an inadvertent shock while in direct or indirect contact with a patient during defibrillation. New evidence suggests that it might even be electrically safe for the rescuer to continue chest compressions during defibrillation if self-adhesive defibrillation electrodes are used and examination gloves are worn. This paper reviews the existing evidence, but warns more definite data are needed to make absolutely sure that there is no risk before defibrillation safety recommendations are changed.

Is external defibrillation an electric threat for bystanders?
Resuscitation. 2009 Apr;80(4):395-401

Transfusion and ARDS

Blood transfusion in trauma is a risk factor for acute respiratory distress syndrome (ARDS). An analysis of 14070 patients in a trauma database showed that 521 (4.6%) developed ARDS. Logisitc regression analysis demonstrated that, independent of injury type, injury severity, or pneumonia, (1) early PRBCs transfusion of more than 5 units during the first 24 h of hospital admission predicted ARDS and (2) each unit of PRBCs transfused early after admission increased the risk of ARDS by 6%.

Early packed red blood cell transfusion and acute respiratory distress syndrome after trauma.
Anesthesiology. 2009 Feb;110(2):351-60

Delays to neurosurgery

Further evidence from the UK shows that patients with acute traumatic brain injury suffer delays in the neurosurgical evacuation of intracranial haematomas which are increased from an average of 3.7 hours to 5.4 hours if they have to undergo interhospital transfer. Coordinated regional trauma systems please!

A prospective study of the time to evacuate acute subdural and extradural haematomas.
Anaesthesia. 2009 Mar;64(3):277-81

Ventilator-associated tracheobronchitis

Ventilator associated pneumonia (VAP) is a well recognised complication of ICU care, but colonisation and infection further up the respiratory tract may be a risk factor for VAP that is worth identifying and treating. Ventilator-associated tracheobronchitis (VAT) has similar diagnostic criteria to VAP, but without the radiographic infiltrates.

Ventilator-associated tracheobronchitis: the impact of targeted antibiotic therapy on patient outcomes
Chest. 2009 Feb;135(2):521-8


oxygen for myocardial infarction – harmful?

Hyperoxia may reduce coronary artery blood flow, increase systemic vascular resistance, and decrease cardiac output. This paper argues that if the baseline arterial oxygen saturations are >90%, high concentration oxygen does not increase oxygen transport, as the reductions in cardiac output are in excess of the increase in oxygen content. The balance of the limited evidence that exists suggests that the routine use of oxygen in uncomplicated MI (no failure or shock) may increase infarct size and possibly increase the risk of mortality, owing to its haemodynamic effects, including a reduction in coronary blood flow.

Routine use of oxygen in the treatment of myocardial infarction: systematic review
Heart. 2009 Mar;95(3):198-202


End expiratory occlusion

OBJECTIVE: During mechanical ventilation, inspiration cyclically decreases the left cardiac preload. Thus, an end-expiratory occlusion may prevent the cyclic impediment in left cardiac preload and may act like a fluid challenge. We tested whether this could serve as a functional test for fluid responsiveness in patients with circulatory failure.

DESIGN: Prospective study.

SETTING: Medical intensive care unit.

PATIENTS: Thirty-four mechanically ventilated patients with shock in whom volume expansion was planned.

INTERVENTION: A 15-second end-expiratory occlusion followed by a 500 mL saline infusion.

MEASUREMENTS: Arterial pressure and pulse contour-derived cardiac index (PiCCOplus) at baseline, during passive leg raising (PLR), during the 5-last seconds of the end-expiratory occlusion, and after volume expansion.

MAIN RESULTS: Volume expansion increased cardiac index by >15% (2.4 +/- 1.0 to 3.3 +/- 1.2 L/min/m, p < 0.05) in 23 patients ("responders"). Before volume expansion, the end-expiratory occlusion significantly increased arterial pulse pressure by 15% +/- 15% and cardiac index by 12% +/- 11% in responders whereas arterial pulse pressure and cardiac index did not change significantly in nonresponders. Fluid responsiveness was predicted by an increase in pulse pressure >or=5% during the end-expiratory occlusion with a sensitivity and a specificity of 87% and 100%, respectively, and by an increase in cardiac index >or=5% during the end-expiratory occlusion with a sensitivity and a specificity of 91% and 100%, respectively. The response of pulse pressure and cardiac index to the end-expiratory occlusion predicted fluid responsiveness with an accuracy that was similar to the response of cardiac index to PLR and that was significantly better than the response of pulse pressure to PLR (receiver operating characteristic curves area 0.957 [95% confidence interval [CI:] 0.825-0.994], 0.972 [95% CI: 0.849-0.995], 0.937 [95% CI: 0.797-0.990], and 0.675 [95% CI: 0.497-0.829], respectively).

CONCLUSIONS:The hemodynamic response to an end-expiratory occlusion can predict volume responsiveness in mechanically ventilated patients.

Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated intensive care unit patients.
Crit Care Med. 2009 Mar;37(3):951-6

Dexmedetomidine vs midazolam

An industry-sponsored double-blind randomised controlled trial comparing midazolam with the central alpha-2 agonist dexmedetomidine showed the newer drug to provide similar levels of sedation with less delirium and a shorter time to extubation. It was associated with more episodes of bradycardia not requiring intervention.
This new sedative drug, related to clonidine, provides some analgesia and anxiolysis, and is noted for its lack of respiratory depression. An accompanying editorial points out the known association between benzodiazepines and delirium, and asks whether a comparison with propofol would have shown the same improved outcomes.
Dexmedetomidine vs midazolam for sedation of critically ill patients: a randomized trial
JAMA. 2009 Feb 4;301(5):542-4

Neonatal prostaglandin E1 and apnoea

The risk of apnoea in neonates requiring prostaglandin E1 infusions for duct-dependent congenital heart disease is well described and often results in the recommendation to intubate prior to transfer. An American study of 202 transported infants on PGE1 shows a higher rate of transport-related complications in those that had been intubated. None of the 73 (36%) unintubated patients required intubation for apneoa during transport. These data are in keeping with a previous Australian study of 300 infants receiving PGE1 in which only 2 of 78 unintubated patients experienced apnoea.
To intubate or not to intubate? Transporting infants on prostaglandin E1
Pediatrics. 2009 Jan;123(1):e25-30

Failed prehospital intubation attempts and pneumonitis

A review of 1954 out-of-hospital tracheal intubation (ETI) attempts by EMS crews revealed 444 (22.7%) patients experienced one or more ETI errors, including tube misplacement or dislodgement in 61 (3%), multiple ETI attempts in 62 (3%) and failed ETI in 359 (15%). Pneumonitis was associated with failed ETI (n=20, 19%; univariable OR 2.54; 95% CI 1.24-5.25). The authors conclude that out-of-hospital ETI errors are not associated with mortality, but failed out-of-hospital ETI increases the odds of pneumonitis.