Israel Medical Association Journal

Background: Diabetic ketoacidosis (DKA) is a common and serious complication of diabetes mellitus (DM).

Objectives: To evaluate the clinical characteristics, hospital management and outcomes of patients with DKA.

Methods: We performed a retrospective cohort study of patients hospitalized with DKA during the period 1 January 2003 to 1 January 2010. Three groups were compared: patients with mild DKA, with moderate DKA, and with severe DKA. The primary outcome was in-hospital all-cause mortality. The secondary outcomes were 30 days all-cause mortality, length of hospital stay, and complication rate.

Results: The study population comprised 220 patients with DKA. In the mild (78 patients) and moderate (116 patients) groups there was a higher proportion of patients with type 1 DM (75.6%, 79.3%) compared with 57.7% in the severe group (26 patients, P = 0.08). HbA1C levels prior to admission were high in all three groups, without significant difference (10.9 ± 2.2, 10.7 ± 1.9, and 10.6 ± 2.4 respectively, P = 0.9). In all groups the most frequent precipitating factors were related to insulin therapy and infections. The patients with severe DKA had more electrolyte abnormalities (hypokalemia, hypomagnesemia, hypophosphatemia) compared with the mild and moderate forms of the disease. While 72.7% of the entire cohort was hospitalized in the general medical ward, 80.8% of those with severe DKA were admitted to the intensive care unit. The in-hospital mortality rate for the entire cohort was 4.1%, comparable with previous data from experienced centers. Advanced age, mechanical ventilation and bedridden state were independent predictors associated with 30 day mortality: hazard ratio (HR) 1.1, 95% confidence interval (CI) 1.02–1.11; HR 6.8, 95% CI 2.03–23.1; and HR 3.8, 95% CI 1.13–12.7, respectively.

Conclusions: Patients with DKA in our study were generally poorly controlled prior to their admission, as reflected by high HbA1c levels. Type 2 DM is frequently associated with DKA including the severe form of the disease. The most common precipitating factors for the development of DKA were related to insulin therapy and infections. Advanced age, mechanical ventilation and bedridden state were independent predictors of 30 day mortality.
 

Background: The most common and most serious complication of varicella (chickenpox) in adults is pneumonia, which can lead to severe respiratory failure. Varicella pneumonia is associated with considerable morbidity and even death.

Objectives: To summarize our experience with varicella pneumonia in terms of clinical, laboratory and radiological characteristics as well as risk factors, management and outcome.

Methods: We conducted a retrospective cohort survey in our facility from 1995 to 2008.

Results: Our cohort comprised 21 patients with varicella pneumonia, of whom 19 (90%) were men; their mean age was 35 ± 10.5 years. Nineteen patients (90%) were Bedouins and 18 (86%) were smokers. Eleven (52%) were admitted to the Medical Intensive Care Unit; 3 of them required mechanical ventilation and the remaining 10 (48%) were admitted to the general medical ward. Median length of stay was 6 ± 7.7 days. Hypoxemia and elevated lactate dehydrogenase on admission were associated with respiratory failure. Radiological manifestations were variable and nine patients exhibited characteristic findings. All but one patient were treated with acyclovir. All patients fully recovered.

Conclusions: In southern Israel varicella pneumonia is primarily a disease of young male Bedouins who are smokers. Severity ranges from mild disease to severe, resulting at times in respiratory failure requiring mechanical ventilation. Prognosis is favorable with complete recovery.

Background: The Dead Sea in Israel has a very high mineral content. Near-drowning in the Dead Sea is expected to result in severe electrolyte abnormalities and respiratory failure. Previous limited studies reported a high mortality rate.

Objective: To evaluate the clinical and biochemical manifestations and disease outcome of near-drowning in the Dead Sea.

Methods: Data were abstracted from the archives of Soroka University Medical Center. The cohort comprised 69 patients who nearly drowned in the Dead Sea.

Results: The median age of the patients was 68 years (range 21–84). There were two major manifestations of near-drowning in the Dead Sea: electrolyte imbalance and acute lung injury. Serum calcium, magnesium and phosphorus (but not sodium, potassium and chloride) were abnormal in most patients. Median serum electrolyte levels (and range) on admission were 10.9 mEq/dl (9–24) for calcium, 4.3 mEq/dl (1–30) for magnesium, and 4.1 mEq/dl (2–9) for phosphorus. These levels quickly normalized with forced diuresis within 24 hours. Acute lung injury – namely, hypoxic bilateral pneumonitis – occurred in 29 patients. Mechanical ventilation was required in 11 patients. Sixty-five patients recovered fully, while the remaining 4 had minor sequelae.

Conclusions: Near-drowning in the Dead Sea is a syndrome of severe electrolyte abnormalities and lung injury. Early treatment, with forced diuresis and supportive care, results in prompt recovery.

Sepsis is an infection-induced inflammatory syndrome that results in a complex network of adaptive and maladaptive alterations in homeostatic mechanisms. Severe sepsis, defined as sepsis associated with acute organ failure, is a serious disease with a mortality rate of 30–50%. The coagulation system, through complex interactions, has an important role in the final outcome of the sepsis-induced inflammatory cascade. A fine and delicate balance that normally exists between anticoagulant mechanisms and the procoagulant response is altered in sepsis. Activated protein C, an endogenous vitamin K-dependent anticoagulant, plays a major role in the down-regulation of the procoagulant arm. It also possesses anti-inflammatory properties. Endothelial damage during sepsis impairs the endothelium-dependent activation of protein C, thus shifting the balance towards thrombosis. This shift may contribute to the development of sepsis-related multi-organ failure. Evidence suggesting that activation of the coagulation system may contribute to sepsis-related morbidity and mortality has led to extensive research attempting to correct the hemostatic defects seen in septic patients. Indeed, a recent randomized controlled trial demonstrated a reduction in overall mortality in patients with severe sepsis treated with APC[1]. In this review we discuss the pathogenesis of the coagulopathy of sepsis, as well as the new therapeutic approaches aimed at correcting the defects in the coagulation system.

Patients with a compromised immune system suffer a wide variety of insults. Interstitial lung changes are one of the most common and serious complications in this group of patients. The morbidity rate reaches 50% and up to 90% if endotracheal intubation and mechanical ventilation are necessary. Opportunistic and bacterial infections are common causes of pulmonary infiltrates and must be distinguished from other conditions such as drug reactions, volume overload, pulmonary hemorrhage, and malignant diseases. Accurate and prompt diagnosis of potentially treatable causes can be life-saving. Non-invasive diagnostic methods for evaluation are often of little value, and an invasive procedure - such as bronchoalveolar lavage, transbronchial biopsy or even open lung biopsy - is therefore performed to obtain a histologic diagnosis. Yet, even when a specific diagnosis is made it may not improve the patient’s survival. Numerous textbook and review articles have focused on the management of this condition. The present review attempts to provide a comprehensive and systematic picture of current knowledge and an integrated approach to these challenging patients.

Sepsis is an inflammatory syndrome caused by infection. Consequently, anti-inflammatory therapies in sepsis have been a subject of extensive research and corticosteroids have been used for years in the therapy of severe infections. However, studies conducted in the 1980s failed to demonstrate any beneficial effects of high dose, short-term steroid therapy in sepsis and this therapy was therefore abandoned during the last decade. Recently, a new concept has emerged with more promising results - low dose, long-term hydrocortisone therapy – and this approach is now being evaluated in the treatment of septic shock. It is supported by the observation that many sepsis patients have relative adrenal insufficiency. Moreover, the anti-inflammatory effects of steroids and their ability to improve reactivity to catecholamines further contribute to their effects in sepsis. Large randomized clinical trials will be required to determine the exact role of corticosteroids in septic shock.