Phosphate induced crystal acute kidney injury - an under-recognized cause of acute kidney injury potentially leading to chronic kidney disease: case report and review of the literature.

Acute phosphate nephropathy or nephrocalcinosis is a tubulointerstitial nephropathy characterized by tubular calcium phosphate deposition - crystal nephropathy - and slowly progressive renal insufficiency during or following treatment with preparations containing sodium phosphate. We report a patient who developed nephrocalcinosis (crystal induced acute kidney injury) following the administration of a combination of oral and rectal sodium phosphate for treatment of postoperative constipation. A timely renal replacement therapy procedure may reverse the process of crystallization and the irreversible slope towards chronic dialysis.

Handling continuous renal replacement therapy-related adverse effects in intensive care unit patients: the dialytrauma concept.

Continuous renal replacement therapy (CRRT) is increasingly used for the management of critically ill patients. As a consequence, the incidence of complications that accompany CRRT is also rising. However, a standardized approach for preventing or minimizing these adverse events is lacking. Dialytrauma is a newly proposed concept that encompasses all harmful adverse events related to CRRT while providing a framework for prevention or, at the least, early recognition of these events in order to attenuate the consequences. A mainstay of this approach is the utilization of a dedicated checklist for improving CRRT quality and patient safety. In this context, we discuss the most important adverse effects of CRRT and review current strategies to minimize them.

Sudden cardiac arrest during pregnancy: a rare complication of acquired maternal diaphragmatic hernia.

Acute cardiac arrest during pregnancy is a rare but devastating event. Major causes are haemorrhagic, septic or anaphylactic shock, trauma, pulmonary or amniotic fluid embolism, and congenital or acquired cardiac disease. We present a case of massive intrathoracic migration of viscera through a left diaphragmatic hernia in a pregnant multipara, causing acute obstructive shock and cardiac arrest. Complications of intrathoracic herniation occur when the intruding viscera cause left lung and cardiac compression or mediastinal "tamponade" with decreased venous return. Intrathoracic strangulation of viscera is also common and may cause ischaemia, gangrene and eventual perforation. Sudden cardiac arrest as first sign of left diaphragmatic rupture during pregnancy, however, has rarely been described. In contrast with our patient, this catastrophic event is mostly seen in nulli- and primipara with a known congenital left diaphragmatic defect. Management of a diaphragmatic hernia depends on the clinical presentation and the period of gestation during which it is detected. Despite prolonged resuscitation with more than 1 hour of chest compressions, our patient recovered completely.

New insights regarding rationale, therapeutic target and dose of hemofiltration and hybrid therapies in septic acute kidney injury.

Mediator removal from tissue (capillary blood compartment, CABC) and transport to the central circulation (central blood compartment, CEBC) must be effective. Effectiveness through a passive mechanism seems unlikely as the surface of CEBC (30 m(2)) is smaller than CABC (300 m(2)) whereby the former will be a limiting factor in passive transport. According to studies, a high exchange volume can induce an 80-fold increase in lymphatic flow. This results in displacement (active transport) of mediators to CEBC. Recent studies have shown that the delivered dose constitutes the mainstay of continuous renal replacement therapy. However, these results are not likely to change the recommendation: 35 ml/kg/h, adjusted for predilution, in septic acute kidney injury (AKI). Recently, studies were focusing on global intensive care unit AKI. In non-septic AKI, those studies show that 20-25 ml/kg/h was optimal. The DO-RE-MI trial underscored the importance of delivery which could be obtained by targeting doses between 5 and 10 ml/kg/h higher than prescribed. Until the IVOIRE trial becomes available, septic AKI should be treated by continuous veno-venous hemofiltration at 35 ml/kg/h. In non-septic AKI, 25 ml/kg/h remains optimal.

Septic acute kidney injury: the culprit is inflammatory apoptosis rather than ischemic necrosis.

For a long time, acute kidney injury (AKI) was considered to be a primarily hemodynamic condition characterized by a reduction of renal blood flow, induced by either cardiogenic or distributive (septic) shock. Consequently, all efforts to treat AKI were essentially concentrated on increasing renal flow by enhancing cardiac flow output and perfusion pressure. At the beginning of this decade, Bellomo and co-workers produced new and intriguing data in an animal model of septic AKI that undermined existing concepts. They observed that medullar and cortical renal blood flow were both maintained and even increased in septic shock, underscoring that septic AKI was a totally different physiological phenomenon than nonseptic AKI. Also, apoptosis was found to play a more important role in sepsis and septic shock than pure necrosis. Despite these findings, the role of apoptosis as a main mechanism of organ dysfunction remains topic of debate.

Diagnostic markers of sepsis in the emergency department.

Sepsis is defined as the systemic inflammatory response to infection. However, changes in body temperature, heart and respiratory rate and white cell count (the "SIRS" criteria) are not specific enough to identify infected patients in the emergency department. Among many biological parameters, measurement of lactate, central venous oxygen saturation (ScvO2), C-reactive protein (CRP) and procalcitonin (PCT) are of particular interest. Early (within 6h) and goal-directed (ScvO2 > 70%) resuscitation increases survival in severe sepsis and septic shock, particularly in patients with high lactate clearances. CRP and PCT are both useful markers of sepsis but PCT increases earlier, better differentiates infective from non-infective causes of inflammation, more closely correlates with sepsis severity in terms of shock and organ dysfunction and better predicts outcome when followed in time. However, PCT measurement is more costly, time-consuming, and not widespread available. New markers for rapid diagnosis of sepsis (e.g. TREM-1) are under investigation.

A prospective, open, single blind, randomized study comparing four analgesics in the treatment of peripheral injury in the emergency department.

The efficacy of four analgesics, distinct concerning analgesic power and mechanism of action, was evaluated for pain relief in patients suffering from single peripheral injury. Patients were randomly allocated to receive either propacetamol (the pro-drug of paracetamol) 20 mg/kg i.v., piritramide 0.25 mg/kg i.m., tramadol 1 mg/kg i.v. or diclofenac 1 mg/kg i.v. Pain scores were measured by the patient using the visual analogue scale (VAS) and by an observer using a 4-point verbal rating scale (VRS). Cardiorespiratory variables and side effects were recorded. One hundred and sixty patients were included, 131 completed the study. Groups matched for demography and baseline pain levels. In general pain scores decreased with time. No significant differences were found between groups at any particular time point. VAS scores were significantly (p < 0.02) lower than baseline scores 30 minutes after injection in all treatment groups except for the piritramide group where significance (p < 0.01) was reached after 60 minutes. VRS score analysis showed a similar trend although significances differed. In the piritramide group significantly more side effects were noted than in the other groups (p < 0.05). We conclude that intravenous propacetamol, tramadol and diclofenac are equally efficacious for emergency analgesic treatment of single peripheral trauma.

Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock.

BACKGROUND: Cardiac depression in severe sepsis and septic shock is characterized by left ventricular (LV) failure. To date, it is unclear whether clinically unrecognized myocardial cell injury accompanies, causes, or results from this decreased cardiac performance. We therefore studied the relationship between cardiac troponin I (cTnI) and T (cTnT) and LV dysfunction in early septic shock. METHODS: Forty-six patients were consecutively enrolled, fluid-resuscitated, and treated with catecholamines. Cardiac markers were measured at study entry and after 24 and 48 h. LV function was assessed by two-dimensional transesophageal echocardiography. RESULTS: Increased plasma concentrations of cTnI (>/=0.4 microgram/L) and cTnT (>/=0.1 microgram/L) were found in 50% and 36%, respectively, of the patients at one or more time points. cTnI and cTnT were significantly correlated (r = 0.847; P <0.0001). Compared with cTnI-negative patients, cTnI-positive subjects were older, presented higher Acute Physiology and Chronic Health Evaluation II scores at diagnosis, and tended to have a worse survival rate and a more frequent history of arterial hypertension or previous myocardial infarction. In contrast, the two groups did not differ in type of infection or pathogen, or in dose and type of catecholamine administered. Continuous electrocardiographic monitoring in all patients and autopsy in 12 nonsurvivors did not disclose the occurrence of acute ischemia during the first 48 h of observation. LV dysfunction was strongly associated with cTnI positivity (78% vs 9% in cTnI-negative patients; P <0.001). In multiple regression analysis, both cTnI and cTnT were exclusively associated with LV dysfunction (P <0.0001). CONCLUSIONS: These findings suggest that in septic shock, clinically unrecognized myocardial cell injury is a marker of LV dysfunction. The latter condition tends to occur more often in severely ill older patients with underlying cardiovascular disease. Further studies are needed to determine the extent to which myocardial damage is a cause or a consequence of LV dysfunction.

Splenic abscess with Clostridium novyi bacteraemia and sepsis.

Splenic abscess is an uncommon entity and usually results in the death of the patient when left undiagnosed. A case is presented where bacteraemia with an anaerobic Gram-positive bacillus was associated with splenic abscess. Despite treatment with splenectomy and antibiotics the patient developed a multiple organ dysfunction syndrome (MODS) and died. Of particular interest was the isolation of Clostridium novyi type A from the blood in a patient without gas gangrene but with splenic suppuration.

Combined intoxication with a tricyclic antidepressive agent and a neuroleptic.

We report the case of a patient who co-ingested a tricyclic antidepressant (2500 mg of doxepin) and a neuroleptic drug (3500 mg of prothipendyl). Following overdose either agent can affect the central nervous and cardiovascular systems, inducing arrhythmias, conduction disturbances and hypotension. The presented case illustrates that a combined overdose of tricyclic antidepressants and neuroleptics enhances the possible toxic effects of each drug and especially the risk for adverse cardiac events. The clinical features and management of this combined intoxication are discussed. Treatment with sodium bicarbonate readily corrected a potentially life-threatening cardiac arrhythmia and is therefore suggested to be imperative in the treatment of these cases.

Reversible cardiac failure in an adolescent after prolonged exposure to carbon monoxide.

We describe the case of an adolescent who developed a severe but fully reversible cardiac dysfunction with low blood levels of carboxy haemoglobin (COHb = 10%) after a prolonged exposure to carbon monoxide. A 15-year-old male was admitted with a Glasgow Coma Scale of 8/15 with suspected postictal state and postanoxic encephalopathy. The cardiorespiratory failure which he developed soon after admission mandated mechanical ventilation, inotropic support and ultimately left ventricular support by intra-aortic balloon counterpulsation. The cardiac dysfunction was documented by radionuclide imaging and echocardiography. The patient fully recovered without neurological deficit. A low blood COHb concentration is a poor safety indicator since high tissue levels of accumulated carbon monoxide can be associated with coma and fulminant cardiorespiratory failure requiring advanced life support facilities.

Gastric emptying in critically ill patients is accelerated by adding cisapride to a standard enteral feeding protocol: results of a prospective, randomized, controlled trial.

OBJECTIVE: To investigate the effect of cisapride, a relatively new prokinetic agent, on gastric emptying in critically ill patients. DESIGN: Prospective, randomized, controlled study. SETTING: Adult medical/surgical intensive care unit in a university hospital. PATIENTS: Twenty-one consecutively enrolled patients, requiring prolonged mechanical ventilation and enteral feeding. INTERVENTIONS: Patients were randomized to receive either no cisapride or 10 mg of cisapride four times daily, which was added to a standard enteral nutrition feeding protocol. MEASUREMENTS AND MAIN RESULTS: Gastric emptying was evaluated by daily measurements of gastric residue and on days 5 through 7 by bedside scintigraphy. Normal values for gastric clearance of a tracer-labeled test meal and for measurements obtained in the supine position were determined in ten healthy volunteers. The mean time at which 50% of the technetium 99m-labeled test meal was eliminated from the stomach (T 1/2) in this control group was 31 +/- 15 mins. In ten critically ill patients (enteral nutrition group), gastric emptying was markedly delayed after 5 to 7 days of enteral feeding (mean T 1/2 = 78 +/- 40 mins; p < .002 as compared with the control group). In contrast, patients treated with cisapride (cisapride group) showed an accelerated gastric emptying (mean T 1/2 = 18 +/- 7 mins; p > .05 as compared with controls; p < .005 as compared with enteral nutrition group). The mean gastric residue over a 1-wk period was also significantly lower in the cisapride group than in the enteral nutrition group (17.7 +/- 8.9 vs. 94.5 +/- 33.4 mL; p < .001). CONCLUSIONS: The data indicate that gastric emptying in critically ill, sedated, and mechanically ventilated patients can be significantly improved by adding cisapride to a routine enteral feeding protocol.

Bedside evaluation of intraocular pressure in critically ill patients, ventilated at different levels of positive end-expiratory pressure.

Animal experiments suggest that the application of positive end-expiratory pressure (PEEP) levels > or = 10 cm H2O increase intraocular pressure (IOP), probably through ophthalmic and episcleral venous outflow obstruction secondary to PEEP-induced increase in central venous pressure (CVP). To evaluate whether a similar response occurs in humans, we studied the effects of varying levels of PEEP on IOP in 11 critically ill sedated and mechanically ventilated patients, aged 35 to 88 yrs (mean: 68 yrs), without evidence of ocular disease. Measured variables included PaCO2, PaO2, mean arterial pressure (MAP), CVP and IOP, and were recorded at zero end-expiratory pressure and at 5, 10 and 15 cm H2O PEEP, applied in random order. IOP was measured by the same investigator at the bedside, using a portable and battery-operated tonometer (Tono-Pen). As expected, PaO2 increased significantly from baseline at all PEEP levels. At the three levels of PEEP, no significant change of PaCO2 from its corresponding baseline values was observed. At 5 cm H2O PEEP neither CVP nor IOP raised significantly from baseline. IOP increased significantly (p < 0.01) from 12 +/- 4 to 14 +/- 4 mmHg at 10 cm H2O PEEP and from 13 +/- 4 to 16 +/- 5 mmHg at 15 cm H2O PEEP. CVP also increased significantly (p < 0.01) and in parallel with IOP at 10 and 15 cm H2O PEEP. Since IOP tends to rise significantly when PEEP levels exceed 10 cm H2O, PEEP-ventilated patients in whom such increase is undesirable might benefit from regular bedside IOP monitoring.

Passive immunotherapy of gram-negative bacteremia, sepsis and septic shock.

Despite the use of increasingly potent antibiotics and aggressive cardiovascular monitoring and support, Gram-negative bacteremia and ensuing sepsis and septic shock remain a leading cause of morbidity and mortality after surgery and in critically ill patients. In previous years several new agents and techniques have been developed to improve management and outcome of severe Gram-negative infections. A recently introduced treatment is passive immunotherapy by administration of poly- or monoclonal anti-endotoxin antibodies. The current view--sustained by experimental and human studies--on the mechanism of protection afforded by immunotherapy is that the harmful effects of endotoxin are neutralized by cross-reactive antibodies to the core glycolipid structure of rough mutant Gram-negative bacilli. Two recent large clinical trials reported impressive results achieved through the use of monoclonal anti-endotoxin antibodies in certain subgroups of patients with Gram-negative sepsis. However, this treatment is empirical, expensive and it does not affect overall sepsis mortality. Cytokines such as tumor necrosis factor alpha and interleukin-1 play a pivotal role in sepsis. Experimental studies suggest that specific antagonism of these mediators might offer great perspectives for the treatment of Gram-negative sepsis. An early multi-pharmacological approach aimed at interruption of multiple steps underlying the inflammatory septic cascade will probably constitute the most promising future treatment of severe Gram-negative infectious disease.

Splenic abscess: a diagnostic challenge.

Splenic abscess is uncommon and remains a diagnostic challenge. We present two cases. Both patients had predisposing factors that may have led to the splenic abscess. At admission, both patients presented clinical and roentgenographic signs, suggestive but nonspecific for splenic suppuration. Of particular interest was the isolation of Salmonella typhimurium in our first patient. The literature on splenic abscess is reviewed.

An unusual case of cystic lymphangiomatosis of the spleen.

Isolated lymphangiomatosis of the spleen is rare. When present, it is usually considered to be accompanied by splenomegaly. We describe a case of cystic lymphangiomatosis in a patient with a normal-sized spleen. While ultrasound, angiography and computed tomography are considered to complement each other in reaching a preoperative diagnosis of splenic lymphangiomatosis, in the present case, magnetic resonance imaging proved to be an additional helpful non-invasive diagnostic method.