John Botha

High-flow nasal oxygen vs high-flow face mask: A randomized crossover trial in extubated patients

PURPOSE Oxygen delivery after extubation is critical to maintain adequate oxygenation and to avoid reintubation. The delivery of oxygen in such situations is usually by high-flow face mask (HFFM). Yet, this may be uncomfortable for some patients. A recent advance in oxygen delivery technology is high-flow nasal prongs (HFNP). There are no randomized trials comparing these 2 modes. METHODS Patients were randomized to either protocol A (n = 25; HFFM followed by HFNP) or protocol B (n = 25; HFNP followed by HFFM) after a stabilization period of 30 minutes after extubation. The primary objective was to compare the efficacy of HFNP to HFFM in maintaining gas exchange as measured by arterial blood gas. Secondary objective was to compare the relative effects on heart rate, blood pressure, respiratory rate, comfort, and tolerance. RESULTS Patients in both protocols were comparable in terms of age, demographic, and physiologic variables including arterial blood gas, blood pressure, heart rate, respiratory rate, Glasgow Coma Score, sedation, and Acute Physiology and Chronic Health Evaluation (APACHE) III scores. There was no significant difference in gas exchange, respiratory rate, or hemodynamics. There was a significant difference (P = .01) in tolerance, with nasal prongs being well tolerated. There was a trend (P = .09) toward better patient comfort with HFNP. CONCLUSIONS High-flow nasal prongs are as effective as HFFM in delivering oxygen to extubated patients who require high-flow oxygen. The tolerance of HFNP was significantly better than in HFFM.

Hypothermia predicts mortality in critically ill elderly patients with sepsis

BackgroundAdvanced age is one of the factors that increase mortality in intensive care. Sepsis and multi-organ failure are likely to further increase mortality in elderly patients.We compared the characteristics and outcomes of septic elderly patients (> 65 years) with younger patients (≤ 65 years) and identified factors during the first 24 hours of presentation that could predict mortality in elderly patients.MethodsThis study was conducted in a Level III intensive care unit with a case mix of medical and surgical patients excluding cardiac and neurosurgical patients.We performed a retrospective review of all septic patients admitted to our ICU between July 2004 and May 2007. In addition to demographics and co-morbidities, physiological and laboratory variables were analysed to identify early predictors of mortality in elderly patients with sepsis.ResultsOf 175 patients admitted with sepsis, 108 were older than 65 years. Elderly patients differed from younger patients with regard to sex, temperature (37.2°C VS 37.8°C p < 0.01), heart rate, systolic blood pressure, pH, HCO3, potassium, urea, creatinine, APACHE III and SAPS II. The ICU and hospital mortality was significantly higher in elderly patients (10.6% Vs 23.14% (p = 0.04) and 19.4 Vs 35.1 (p = 0.02) respectively). Elderly patients who died in hospital had a significant difference in pH, HCO3, mean blood pressure, potassium, albumin, organs failed, lactate, APACHE III and SAPS II compared to the elderly patients who survived while the mean age and co-morbidities were comparable. Logistic regression analysis identified temperature (OR [per degree centigrade decrease] 0.51; 95% CI 0.306- 0.854; p = 0.010) and SAPS II (OR [per point increase]: 1.12; 95% CI 1.016-1.235; p = 0.02) during the first 24 hours of admission to independently predict increased hospital mortality in elderly patients.ConclusionsThe mortality in elderly patients with sepsis is higher than the younger patients. Temperature (hypothermia) and SAPS II scores during the first 24 hours of presentation independently predict hospital mortality.

End of life management of adult patients in an Australian metropolitan intensive care unit: A retrospective observational study.

BACKGROUND Death in the intensive care unit is often predictable. End of life management is often discussed and initiated when futility of care appears evident. Respect for patients wishes, dignity in death, and family involvement in the decision-making process is optimal. This goal may often be elusive. PURPOSE Our purpose was to review the end of life processes and family involvement within our Unit. METHODS We conducted a chart audit of all deaths in our 10 bed Unit over a 12-month period, reviewing patient demographics, diagnosis on admission, patient acuity, expectation of death and not-for-resuscitation status. Discussions with the family, treatments withheld and withdrawn and extubation practices were documented. The presence of family or next-of-kin at the time of death, the time to death after withdrawal of therapy and family concerns were recorded. RESULTS There were 70 patients with a mean age of 69 years. Death was expected in 60 patients (86%) and not-for-resuscitation was documented in 58 cases (85%). Family discussions were held in 63 cases (90%) and treatment was withdrawn in 34 deaths (49%). After withdrawal of therapies, 31 patients (44%) died within 6h. Ventilatory support was withdrawn in 24 cases (36%). Family members were present at the time of death in 46 cases (66%). Family concerns were documented about the end of life care in only 1 case (1.4%). CONCLUSION Our data suggests that death in our Unit was often predictable and that end of life management was a consultative process.

Stress hyperglycemia may not be harmful in critically ill patients with sepsis

BACKGROUND Stress hyperglycemia (SH) is commonly seen in critically ill patients. It has been shown to be associated with adverse outcomes in some groups of patients. The effects of SH on critically ill patients with sepsis have not been well studied. We aimed to evaluate the effects of SH in critically ill patients with sepsis. METHODS In this retrospective study, patients with sepsis admitted to intensive care unit (ICU) over a 5-year period were included. RESULTS Of 297 patients, 204 (68.7%) had SH during the study period. The mean blood glucose level in patients with SH was 8.7 mmol/L compared with 5.9 mmol/L in those without SH (P < .05). There were no statistically significant differences in age; sex; sepsis severity; cardiovascular, respiratory, and renal comorbidities; requirement of mechanical ventilation; inotropes; and Acute Physiology, Age, and Chronic Health Evaluation III and Simplified Acute Physiology 2 scores on ICU admission. Intensive care unit mortality was significantly lower in patients who had SH. The median duration of ICU and hospital length of stay was longer in patients with SH. On logistic regression analysis, the presence of SH was associated with reduced ICU mortality. Subgroup analysis revealed SH to be protective in patients with septic shock. CONCLUSION Stress hyperglycemia may not be harmful in critically ill patients with sepsis. Patients with SH had lower ICU mortality.

Effectiveness of extracorporeal membrane oxygenation when conventional ventilation fails : valuable option or vague remedy?

The mortality and morbidity of patients with severe acute respiratory distress syndrome (ARDS) remains high despite the advances in intensive care practice. The low-tidal-volume ventilation strategy (ARDS net protocol) has been shown to be effective in improving survival. Unfortunately, however, some patients have such severe ARDS that they cannot be managed with the ARDS net strategy. In these patients, rescue therapies such as high-frequency ventilation, prone ventilation, nitric oxide, and extracorporeal membrane oxygenation (ECMO) are considered. The CESAR trial has shown that an ECMO-based protocol improved survival without severe disability as compared with conventional ventilation. The recent increased incidence of severe respiratory failure due to H1N1 influenza pandemic has led to an increased use of ECMO. Although several reports showed ECMO use to be encouraging, some scepticism remains. In this article, we reviewed the usefulness of ECMO in patients with severe ARDS in the light of current evidence.

Diaphragmatic regional displacement assessed by ultrasound and correlated to subphrenic organ movement in the critically ill patients—an observational study

INTRODUCTION The objectives of the study are to identify the most reliably imaged regions of the diaphragm, to evaluate the correlation of movement between different parts of each hemidiaphragm, and to assess the agreement between liver or spleen displacement and movement of the ipsilateral hemidiaphragm. METHODS Images of the diaphragm, liver, and spleen were obtained using 2-dimensional ultrasound. Acceptable agreement between regions of the diaphragm, liver, and spleen was defined as an absence of fixed or proportional bias using Deming regression analysis and limits of agreement of 2 SDs of the difference less than 30% of the mean value. RESULTS We included 90 critically ill patients. The medial (87%) and middle (73%) regions of the right hemidiaphragm, liver (87.7%), and spleen (81%) and medial (71%) and middle regions (51%) of the left hemidiaphragm were most frequently imaged. In nonintubated patients, acceptable agreement was present for comparisons of the left middle and medial, right middle and medial, and left middle regions and spleen displacement. In intubated patients and in all patients when combined, acceptable agreement was only present for comparisons of the left middle and medial and right middle and medial regions of the diaphragm. Acceptable agreement was not present for intubated and all patients for diaphragmatic and solid organ movement. CONCLUSION The diaphragm medial part is visualized in the majority of studied patients. The medial and middle thirds may be used interchangeably to assess hemidiaphragm movement. Acceptable agreement does not exist for diaphragm and solid organ movement, other than for the left middle region and the spleen.

Effects of Hypercapnia and Hypercapnic Acidosis on Hospital Mortality in Mechanically Ventilated Patients

Objectives: Lung-protective ventilation is used to prevent further lung injury in patients on invasive mechanical ventilation. However, lung-protective ventilation can cause hypercapnia and hypercapnic acidosis. There are no large clinical studies evaluating the effects of hypercapnia and hypercapnic acidosis in patients requiring mechanical ventilation. Design: Multicenter, binational, retrospective study aimed to assess the impact of compensated hypercapnia and hypercapnic acidosis in patients receiving mechanical ventilation. Settings: Data were extracted from the Australian and New Zealand Intensive Care Society Centre for Outcome and Resource Evaluation Adult Patient Database over a 14-year period where 171 ICUs contributed deidentified data. Patients: Patients were classified into three groups based on a combination of pH and carbon dioxide levels (normocapnia and normal pH, compensated hypercapnia [normal pH with elevated carbon dioxide], and hypercapnic acidosis) during the first 24 hours of ICU stay. Logistic regression analysis was used to identify the independent association of hypercapnia and hypercapnic acidosis with hospital mortality. Interventions: Nil. Measurements and Main Results: A total of 252,812 patients (normocapnia and normal pH, 110,104; compensated hypercapnia, 20,463; and hypercapnic acidosis, 122,245) were included in analysis. Patients with compensated hypercapnia and hypercapnic acidosis had higher Acute Physiology and Chronic Health Evaluation III scores (49.2 vs 53.2 vs 68.6; p < 0.01). The mortality was higher in hypercapnic acidosis patients when compared with other groups, with the lowest mortality in patients with normocapnia and normal pH. After adjusting for severity of illness, the adjusted odds ratio for hospital mortality was higher in hypercapnic acidosis patients (odds ratio, 1.74; 95% CI, 1.62–1.88) and compensated hypercapnia (odds ratio, 1.18; 95% CI, 1.10–1.26) when compared with patients with normocapnia and normal pH (p < 0.001). In patients with hypercapnic acidosis, the mortality increased with increasing PCO2 until 65 mm Hg after which the mortality plateaued. Conclusions: Hypercapnic acidosis during the first 24 hours of intensive care admission is more strongly associated with increased hospital mortality than compensated hypercapnia or normocapnia.

Heparin induced thrombocytopenia in critically ill: Diagnostic dilemmas and management conundrums

Thrombocytopenia is often noted in critically ill patients. While there are many reasons for thrombocytopenia, the use of heparin and its derivatives is increasingly noted to be associated with thrombocytopenia. Heparin induced thrombocytopenia syndrome (HITS) is a distinct entity that is characterised by the occurrence of thrombocytopenia in conjunction with thrombotic manifestations after exposure to unfractionated heparin or low molecular weight heparin. HITS is an immunologic disorder mediated by antibodies to heparin-platelet factor 4 (PF4) complex. HITS is an uncommon cause of thrombocytopenia. Reported incidence of HITS in patients exposed to heparin varies from 0.2% to up to 5%. HITS is rare in ICU populations, with estimates varying from 0.39%-0.48%. It is a complex problem which may cause diagnostic dilemmas and management conundrum. The diagnosis of HITS centers around detection of antibodies against PF4-heparin complexes. Immunoassays performed by most pathology laboratories detect the presence of antibodies, but do not reveal whether the antibodies are pathological. Platelet activation assays demonstrate the presence of clinically relevant antibodies, but only a minority of laboratories conduct them. Several anticoagulants are used in management of HITS. In this review we discuss the incidence, pathogenesis, diagnosis and management of HITS.

Fatal skin and soft tissue infection of multidrug resistant Acinetobacter baumannii: A case report

INTRODUCTION Acinetobacter baumannii is usually associated with respiratory tract, urinary tract and bloodstream infections. Recent reports suggest that it is increasingly causing skin and soft tissue infections. It is also evolving as a multidrug resistant organism that can be difficult to treat. We present a fatal case of multidrug resistant A. baumannii soft tissue infection and review of relevant literature. PRESENTATION OF CASE A 41 year old morbidly obese man, with history of alcoholic liver disease presented with left superficial pre-tibial abrasions and cellulitis caused by multidrug resistant (MDR) A. baumannii. In spite of early antibiotic administration he developed extensive myositis and fat necrosis requiring extensive and multiple surgical debridements. He deteriorated despite appropriate antibiotic therapy and multiple surgical interventions with development of multi-organ failure and died. DISCUSSION Managing Acinetobacter infections remains difficult due to the array of resistance and the pathogens ability to develop new and ongoing resistance. The early diagnosis of necrotizing soft tissue infection may be challenging, but the key to successful management of patients with necrotizing soft tissue infection are early recognition and complete surgical debridement. CONCLUSION A. baumannii is emerging as an important cause of severe, life-threatening soft tissue infections. Multidrug resistant A. baumannii soft tissue infections may carry a high mortality in spite of early and aggressive treatment. Clinicians need to consider appropriate early empirical antibiotic coverage or the use of combination therapy to include MDR A. baumannii as a cause of skin and soft tissue infections.

Can seizures and rhabdomyolysis be a potentially serious complication of hyponatremia due to polydipsia

Patrick Tolan, Denis O’Loughlin and John Botha, Frankston Hospital, Frankston, Australia: We report the case of AB, a 41-year-old single female admitted to the intensive care unit with seizures secondary to severe hyponatremia, who subsequently developed rhabdomyolysis. She had a 10-year history of paranoid schizophrenia. At no time prior to this episode were problems with excessive water intake or hyponatremia noted. In the weeks prior to her admission with seizures she had been receiving assertive community treatment with a case manager visiting daily and monitoring her medication compliance. (Olanzapine 10 mg per day and sertraline 50 mg per day.) In the days prior to her admission she reported that she consumed about 10 glasses of water per day which she said was normal for her. On the morning of her admission she was found at home unconscious and unrouseable and had several generalised tonic-clonic seizures. She was intubated by ambulance staff and transferred to the emergency department. On arrival in the emergency department her Glasgow Coma Score was 3/15. She was hypothermic temperature of 34.8°C, pulse 90 beats per minute and blood pressure 120/70 mmHg. There were no focal neurological signs and with the exception of bi-basal crepitations in the lung fields and a rash on both legs examination was unremarkable. She had a low serum sodium 104 mmol/L (135– 145 mmol/L) and a low urinary osmolarity. A head computerized tomography scan was normal. The differential diagnoses made at initial assessment were a syndrome of inappropriate antidiuretic hormone secretion or water intoxication secondary to psychogenic polydipsia. A low urinary osmolarity, however, made SIADH unlikely. She was transferred to the intensive care department on artificial ventilation with the electrolyte imbalance corrected over the following 48 h with hypertonic saline and diuresis. Creatinine kinase (CK) was normal on admission rising slowly to peak at 91 970 IU/L (1–170 IU/L) on day 5 although there were no other features of neuroleptic malignant syndrome (i.e. no pyrexia, confusion, rigidity or autonomic instability). Creatinine kinase MB fraction troponin and electrocardiogram were all normal. Urinary myoglobin was strongly positive suggesting significant rhabdomyolysis. Despite neuroleptic malignant syndrome being unlikely it was felt prudent to cease both olanzapine and sertraline. During the following 4 days in hospital she remained well, the biochemical abnormalities correcting themselves. She refused inpatient psychiatric admission following discharge from the medical ward and did not satisfy criteria for involuntary treatment at that time. She was discharged home for outpatient follow up on no psychotropic medication and at the time of writing had been re-admitted to hospital for a trial of clozapine. During this admission her serum sodium was within the normal range. If NMS is discounted as playing a role in this case then the cause of the rhabdomyolysis remains unclear. Possibilities are rhabdomyolysis secondary to seizures or dilutional hyponatremia (DH). In the literature there has been a number of reports of rhabdomyolysis secondary to water intoxication. In one case from Japan [1], a 44-year-old woman consumed 3 L of water after drinking alcohol. She became stuporous with sodium of 115 mEq/L and subsequently had a CK rise to 28 560 IU/L. In this case the occurrence of rhabdomyolysis was attributed to water intoxication. In another case also from Japan [2], a 32-year-old woman with schizophrenia had a sodium level of 102 mEq/L and developed a CK of 39 900 on day 5 of admission. The timing of this rise would appear to coincide with that of AB’s present case. Another case from Switzerland was a 42-year-old man with schizophrenia who developed seizures secondary to DH and rhabdomyolysis [3]. These cases indicate that seizures and rhabdomyolysis can be a potentially serious complication of hyponatremia due to polydipsia.