Early surgery in infective endocarditis

Optimal timing of surgical intervention in infective endocarditis is important in reducing mortality. We prospectively studied 126 consecutive episodes of infective endocarditis treated in one institution over 5 years, with special emphasis on long-term results and on the effects on outcome of surgical interventions. Twenty-six patients (21%) underwent acute surgery on median treatment day 14. Mortality during treatment was 8% for patients undergoing acute surgery vs. 11% for those not undergoing surgery, and the adjusted 5-year survival rate of acute surgically treated patients was 91%, compared with 69% for the medically treated patients. Using univariate analysis, excess mortality during 5 years follow-up was associated with new cardiac decompensation at entry (<it>p</it> &lt; 0.01), age (<it>p</it> &lt; 0.01), no acute surgery (<it>p</it> &lt 0.05) and mitral valve involvement (<it>p</it> &lt; 0.05). Multivariate analysis showed new cardiac decompensation at entry to be an independent predictor of cardiac death at 5 years follow-up (relative risk 2.39, CI 1.05-5.45), while no surgery during active disease implied a relative risk of 3.45, though not statistically significant. Patients undergoing surgery very early (&les; 10 days of treatment) did not have a poorer outcome. Acute valve replacement, as compared with medical therapy only, might be important to increase both short-term and long-term survival in infective endocarditis.      

Predictors of outcome in Cryptococcus neoformans var. gattii meningitis

In Papua New Guinea, <it>Cryptococcus neoformans</it> var. <it>gattii</it> meningitis has a high fatality rate even in immunocompetent patients. Our retrospective study attempted to identify marker of poor prognosis. Of 88 immunocompetent patients, 30 (34.1%) died, usually soon after admission, and mortality was higher in men (<it>p</it> = 0.025) and older patients (<it>p</it> = 0.039). Death was associated with altered consciousness (<it>p</it>&lt;0.001), a history of convulsions prior to treatment (<it>p</it> = 0.002) and a maximum systolic blood pressure of &gt;150 mmHg (<it>p</it> = 0.017). These data suggest that death results from raised intracranial pressure and subsequent tentorial herniation. However, CSF opening pressure measured on admission was raised in 29/36 (81%) patients and did not predict outcome. In survivors, relapse was uncommon and was not predicted by discharge serum cryptococcal antigen titres, which were frequently raised on completion of therapy in asymptomatic patients. Mortality may be reduced if efforts are made to lower intracranial pressure in those patients who present with markers of poor prognosis.      

Autoantibodies against bactericidal/permeability-increasing protein in patients with cystic fibrosis

Cystic fibrosis (CF), a genetic disorder, is characterized by chronic pulmonary infection/inflammation which leads to respiratory failure. The presence of anti-neutrophil cytoplasmic autoantibodies (ANCA) has previously been observed in the sera of patients with CF. In view of the known relationship of ANCA with primary vasculitis and of their putative pathogenetic role in these disorders, we studied the presence, specificity and isotype of ANCA and their clinical associations in 66 adult CF patients. None of the 66 CF samples had autoantibodies to the major ANCA antigens, proteinase 3 or myeloperoxidase. However, 60/66 (91%) CF samples contained IgG and 55/66 (83%) IgA, autoantibodies to bactericidal/permeability increasing protein (BPI), a recently characterized ANCA specificity. All the IgA anti-BPI-positive samples were also IgG anti-BPI-positive. The autoantibody specificity was confirmed by inhibition assay and immunoblotting of CF sera against a neutrophil granule preparation. Furthermore, in this cross-sectional study, anti-BPI levels were inversely correlated with the observed reductions in FEV1 and FVC (IgA anti-BPI and FEV1: r = 0.508, <it>p</it> &lt; 0.0001), and both IgG and IgA anti-BPI levels were higher in CF patients with secondary vasculitis (<it>n</it> = 6) than in those without (<it>p</it> &lt; 0.05). ANCA with specificity for BPI were present in the majority of CF sera in this study and autoimmune processes may be associated with the development of pulmonary injury in CF.      

The emerging syndrome of envenoming by the New Guinea small-eyed snake Micropechis ikaheka

The New Guinea small-eyed or Ikaheka snake, <it>Micropechis ikaheka</it>, which occurs throughout New Guinea and some adjacent islands, is feared by the indigenes. The first proven human fatality was in the 1950s and this species has since been implicated in many other cases of severe and fatal envenoming. Reliable attribution of envenoming to this species in victims unable to capture or kill the snake recently became possible by the use of enzyme immunoassay. Eleven cases of proven envenoming by <it>M. ikaheka</it>, with two fatalities, were identified in Papua New Guinea and Irian Jaya. Five patients showed no clinical signs of envenoming by other Australasian elapids: mild local swelling, local lymphadenopathy, neurotoxicity, general myalgia, spontaneous systemic bleeding, incoagulable blood and passage of dark urine (haemoglobinuria or myoglobinuria). Two patients developed hypotension and two died of respiratory paralysis 19 and 38 h after being bitten. <it>In vitro</it> studies indicate that the venom is rich in phospholipase A2, is indirectly haemolytic, anticoagulant and inhibits platelets, but is not procoagulant or fibrinolytic. It shows predominantly post-synaptic neurotoxic and myotoxic activity. Anecdotally, Commonwealth Serum Laboratories' (CSL) death adder antivenom has proved ineffective whereas CSL polyvalent antivenom may be beneficial. Anticholinesterase drugs might prove effective in improving neuromuscular transmission and should be tested in patients with neurotoxic envenoming.      

Genetic analysis of thermolabile methylenetetrahydrofolate reductase as a risk factor for myocardial infarction

Hyperhomocyst(e)inemia is associated with an increased risk of coronary artery disease and myocardial infarction. Both genetic and environmental factors influence the plasma level of homocysteine. One of the metabolic pathways for homocysteine involves the enzyme methylenetetrahydrofolate reductase (MTHFR), which regulates the conversion of homocysteine to methionine. A thermolabile variant of MTHFR is associated with reduced enzyme activity and increased plasma homocysteine levels. Recently, the cause of this variant of MTHFR has been identified as a single base change altering an alanine to a valine residue in the protein. Using a PCR-based assay to distinguish the normal and thermolabile variants of MTHFR in this study, we investigated whether the thermolabile variant is a genetic risk factor for myocardial infarction. In a study of 532 subjects (310 myocardial infarction patients and 222 population-based controls), we found no difference in either MTHFR genotype distribution (<it>p</it> = 0.57) or allele frequencies (<it>p</it> = 0.68) between cases and controls. The allele frequencies of the thermolabile variant were 0.34 and 0.35 in cases and controls, respectively. The age- and sex-stratified odds ratio for risk of myocardial infarction associated with homozygosity for the thermolabile variant was 0.85 (95% CI 0.50-1.50, <it>p</it> = 0.57) and that with carriage of the thermolabile allele was 1.06 (95% CI 0.73-1.52, <it>p</it> = 0.76). The odds ratio remained non-significant when restricted to young subjects (&lt;60 years) or males, and were not influenced by several other risk factors for myocardial infarction considered either singly or in combination. Interestingly, in both cases and controls, there was a trend toward a higher prevalence of hypertension in subjects carrying the normal allele, although as this is a <it>post-hoc</it> finding it needs to be interpreted with caution. The thermolabile variant of MTHFR is not a major risk factor for myocardial infarction and is unlikely to explain a significant proportion of the reported association of hyperhomocyst(e)inemia with coronary artery disease.      

The spectrum of meningitis in a population with high prevalence of HIV disease

We studied the spectrum of meningitis and impact of HIV infection retrospectively (8 months) and prospectively (5 months) in 284 adult patients with meningitis hospitalized in Soweto, South Africa. Tuberculous meningitis (TBM) was the most common cause of meningitis (25.4%) followed by acute bacterial meningitis (ABM; 22.5%), acute viral meningitis (14.1%) and cryptococcal meningitis (13%). The in-hospital mortality was &gt;40% in TBM, ABM, cryptococcal meningitis, the neurosurgery and the parameningeal/parenchymal groups. At least 37.3% of all patients were HIV-seropositive (only 67% of patients were tested). In at least 27% of the study group the meningitis was an AIDS-defining illness (TBM, cryptococcal meningitis). Only 56.2% of patients with ABM has positive cultures (CSF or blood), of which <it>Streptococcus pneumoniae</it> was by far the most frequently found organism (35.8%). The spectrum of meningitis in HIV-affected communities in Africa can be expected to change towards a predominance of TBM and cryptococcal meningitis.      

Treating paracetamol overdose by charcoal haemoperfusion and long-hours high-flux dialysis

After serious paracetamol overdose, charcoal haemoperfusion was used to remove paracetamol from the circulation, aiming to reduce the severity of subsequent hepatic damage. Daily long-hours high-flux dialysis was given to patients with grade III-IV hepatic encephalopathy, and also to those at risk of developing encephalopathy. We reviewed patients treated in this manner who had not received N-acetylcysteine within the first 15 h after overdose. From January 1983 to January 1993, 73 patients with serious paracetamol overdose were seen, of whom 51 received charcoal haemoperfusion and/or high-flux dialysis. Patients who were admitted within the first 42 h after overdose and who received haemoperfusion and/or dialysis had significantly lower peak levels of prothrombin time, bilirubin and creatinine than those who were admitted after 42 h. Mortality was also lower amongst patients admitted before 42 h, at 2/18 (11%) vs. 15/33 (45%), <it>p</it> &lt; 0.05.      

CD4 and total lymphocyte counts as predictors of HIV disease progression

CD4+ T-lymphocyte (CD4) counts are a standard laboratory marker of disease progression in HIV infection, but expense precludes their use in large parts of the world. Total lymphocyte counts (TLC), in contrast, are widely available. We compared CD4 and TLC counts as predictors of developing AIDS or death in 831 HIV-positive out-patients (582 males and 249 females with both homosexual (males, n=316) and heterosexual (n=515) transmission patterns. The first CD4 count &lt;200/&mgr;l and first TLC &lt;1250/&mgr;l predicted similar (p=0.52) survival, irrespective of clinical stage. For each clinical stage, a significant difference in progression to AIDS and mortality was predicted by TLC above or below 1250/&mgr;l (p &lt;0.03). Survival and progression to AIDS occurred at similar rates in patients with a TLC &lt;1250/&mgr;l or a CD4 count &lt;200/&mgr;l (p &gt;0.1), and patients with a TLC &gt;1250/&mgr;l or a CD4 count &gt;200/&mgr;l (p &gt;0.5). A TLC &gt;1250/&mgr;l preceded the development of <it>Pneumocystis carinii</it> pneumonia or cerebral toxoplasmosis in 76% of patients. In this longitudinal study, TLC and CD4 counts were equal predictors of disease progression. A TLC &lt;1250/&mgr;l could be considered an indication for commencing cotrimoxazole prophylaxis.      

The clinical course and management of thoracic empyema

We report a prospective multi-centre study of the clinical course and hospital management of thoracic empyema in 119 patients (mean age 54.8). The commonest presenting symptom was malaise (75%), 55% were febrile; 31% were previously well with no predisposing condition. Initial treatments were antibiotics alone (5), needle aspirations (46), intercostal tube drainage (61), rib resection (3) and decortication (4). Overall, intercostal drainage was used in 77 patients (16 failed aspirations), surgical rib resection in 24 (1 failed aspirations, 20 failed drainage), and surgical decortication in 28 (6 failed aspirations, 17 failed drainage). Only 4 patients received intrapleural fibrinolytic agents. Aspiration and drainage were likely to fail if the empyema was &gt;40% of the hemithorax. Median time from treatment start to discharge was: aspirations, 26 days; drainage, 23 days; resection 11 days; decortication, 12 days. Overall 21 patients died (12 with empyema as the major cause); two had been surgically treated. Mortality correlated with age, diabetes, heart failure, and low serum albumin at admission. Infecting organisms, identified in 109 patients (92%) included anaerobes (37), <it>Str. melleri</it> (36), and <it>Str. pneumoniae</it> (28). Six months after discharge, all but six survivors had regained their previous health.      

Trichinella infection and clinical disease

Trichinellosis is caused by ingestion of insufficiently cooked meat contaminated with infective larvae of <it>Trichinella</it> species. The clinical course is highly variable, ranging from no apparent infection to severe and even fatal disease. We report two illustrative cases of trichinellosis. Returning to Denmark a few days after having eaten roasted pork in the Republic of Serbia, a female patient suffered from severe vomiting, epigastric pain, diarrhoea, and later myalgia, generalized oedema, and prostration. A biopsy showed heavy infestation with <it>Trichinella spiralis</it>, 2000 larvae/g of muscle. Life-threatening cardiopulmonary, renal and central nervous system complications developed. The patient recovered after several months. Her husband, who also ate the pork, did not have clinical symptoms, but an increased eosinophil count and a single larva in a muscle biopsy confirmed infection. The epidemiology, clinical manifestations, diagnosis, treatment and prevention of trichinellosis are reviewed.      

The systemic inflammatory response syndrome as a predictor of bacteraemia and outcome from sepsis

Criteria defining the <it>systemic inflammatory response syndrome</it> (SIRS) were used to assess prospectively 270 clinical episodes in which blood cultures were taken from patients in general medicine. SIRS, severe sepsis and septic shock occurred in 149 (55%), 13 (5%) and 9 (3%) episodes, respectively. However, evidence of organ hypoperfusion indicating severe sepsis was recorded as sought in only 26% of episodes of SIRS. Crude mortality at 28 days increased sequentially as more SIRS criteria were met, rising from 12% in non-SIRS blood culture episodes, to 36% when all four criteria were met. Mortality from severe sepsis and septic shock was 38% and 56%, respectively. In 61/64 (95%) episodes of clinically important bacteraemia, patients fulfilled SIRS criteria when the blood culture was taken. However, the positive predictive value of SIRS for predicting bacteraemia was only 7%. Patients who did not fulfill SIRS criteria when blood cultures were taken were at low risk of bacteraemia and comprised 45% (121/270) of the study population. Three patients in this low-risk group had bacteraemia. Mortality in bacteraemic patients with severe sepsis or septic shock who were initially treated with ineffective antibiotics for up to 48 h was 80%, compared to 42% in those always treated appropriately.      

Color Doppler imaging of the gallbladder wall in acute cholecystitis: sonographic<+>–<+>pathologic correlation

Background: The purpose of this study was to evaluate the usefulness of color Doppler imaging (CDI) in suspected cases of acute cholecystitis. Methods: Twenty-two patients suspected of having acute cholecystitis were prospectively evaluated over a 12-month period using gray-scale and color Doppler technique. Gallbladder wall thickness was greater than 2 mm in all patients included in the study. Pathologic correlation was obtained in 17 patients, with clinical or sonographic follow-up in five for a period of 6<+>–/011001/months. CDI was considered positive only if the mid to fundal wall demonstrated flow. Sonographic Murphy's sign and laboratory values were recorded. Results: Eight patients had acute cholecystitis. All had positive color Doppler flow. Wall thickness in these patients ranged between 4 and 10 mm. Three patients with necrotizing acute cholecystitis had no flow within 6<+>–<+>8-mm walls. Six patients with pathologically proven chronic cholecystitis had no evidence of increased flow within thickened walls. Five patients with presumed chronic cholecystitis (thickened wall without increased color flow) were treated medically, and their symptoms resolved. CDI was more sensitive in predicting acute cholecystitis than was the sonographic Murphy's sign and/or laboratory values. Conclusion: CDI demonstrates hyperemic changes in thickened gallbladder walls and is an important adjunct in the diagnosis of acute cholecystitis. Received: 3 February 1995/Accepted: 24 March 1995     

Fibrodysplasia (myositis) ossificans progressiva: clinicopathological features and natural history

Patients with fibrodysplasia (myositis) ossificans progressiva (FOP) (<it>n</it> = 28) were studied for up to 24 years. All had characteristic short big toes potentially recognizable at birth; there were radiographic changes in the toes, thumbs, cervical spine and metaphyses of the long bones, including exostoses. Ossification in the large skeletal muscles began from birth to 16 years (mean age 4.6 years) initially in 25 patients in the neck and upper spinal muscles, and later around the hips, major joints and jaw. The rate and extent of disability was unrelated to the time of onset. There was no evidence that any form of treatment produced consistent benefit. Despite the unique combination of skeletal abnormalities and ectopic ossification, the first diagnosis in patients with FOP was often wrong and usually delayed after ectopic ossification began (mean 2.7 years, range 0-14). Except where presentation was unusual, such as progressive stiffness, this delay was mainly due to failure to recognize the significance of the abnormal toes. The most frequent erroneous histological diagnoses were soft tissue sarcoma or fibromatosis. This series emphasizes the usually incorrect initial diagnosis, the misinterpretation of the histology, the unpredictable prognosis and the failure of current treatment. Despite its extreme rarity, there is a need for wider knowledge of this condition both to avoid clinical errors and to stimulate research.      

Doxycycline versus azithromycin for treatment of leptospirosis and scrub typhus

Leptospirosis and scrub typhus are important causes of acute fever in Southeast Asia. Options for empirical therapy include doxycycline and azithromycin, but it is unclear whether their efficacies are equivalent. We conducted a multicenter, open, randomized controlled trial with adult patients presenting with acute fever (<15 days), without an obvious focus of infection, at four hospitals in Thailand between July 2003 and January 2005. Patients were randomly allocated to receive either a 7-day course of doxycycline or a 3-day course of azithromycin. The cure rate, fever clearance time, and adverse drug events were compared between the two study groups. A total of 296 patients were enrolled in the study. The cause of acute fever was determined for 151 patients (51%): 69 patients (23.3%) had leptospirosis; 57 patients (19.3%) had scrub typhus; 14 patients (4.7%) had murine typhus; and 11 patients (3.7%) had evidence of both leptospirosis and a rickettsial infection. The efficacy of azithromycin was not inferior to that of doxycycline for the treatment of both leptospirosis and scrub typhus, with comparable fever clearance times in the two treatment arms. Adverse events occurred more frequently in the doxycycline group than in the azithromycin group (27.6% and 10.6%, respectively; P = 0.02). In conclusion, doxycycline is an affordable and effective choice for the treatment of both leptospirosis and scrub typhus. Azithromycin was better tolerated than doxycycline but is more expensive and less readily available.     

Risk factors for acute renal failure in trauma patients

Abstract Objective: To elucidate the risk factors for the development of acute renal failure (ARF) in severe trauma. Design: Prospective observational study. Setting: A general intensive care unit (ICU) of a university hospital. Patients: A cohort of 153 consecutive trauma patients admitted to the ICU over a period of 30 months. Results: Forty-eight (31 %) patients developed ARF. They were older than the 105 patients without ARF (p = 0.002), had a higher Injury Severity Score (ISS) (p < 0.001), higher mortality (p < 0.001), a more compromised neurological condition (p = 0.007), and their arterial pressure at study entry was lower (p = 0.0015). In the univariate analysis, the risk of ARF increased by age, ISS > 17, the presence of hemoperitoneum, shock, hypotension, or bone fractures, rhabdomyolysis with creatine phosphokinase (CPK) > 10 000 IU/l, presence of acute lung injury requiring mechanical ventilation, and Glasgow Coma Score < 10. Sepsis and use of nephrotoxic agents were not associated with an increased risk of ARF. In the logistic model, the need for mechanical ventilation with a positive end-expiratory pressure > 6 cm H₂O, rhabdomyolysis with CPK > 10 000 IU/l, and hemoperitoneum were the three conditions most strongly associated with ARF. Conclusions: The identified risk factors for post-traumatic acute renal failure may help the provision of future strategies. Received: 22 September 1997 Accepted: 14 May 1998     

Early therapeutic plasma exchange may improve treatment outcomes in severe acute toxic Hepatitis

Background and objectivesAcute toxic hepatitis can result in a different clinical course from a completely curable disease to subacute hepatitis, chronic hepatitis, and fulminant hepatitis failure, which is quite mortal. For this purpose, therapeutic plasma exchange (TPE) can be used for improving treatment outcomes by reducing the harmful substances caused with and/or without liver function in acute toxic hepatitis. We aimed to evaluate treatment outcomes in severe acute toxic hepatitis patients who applied early TPE procedure.Materials and MethodsA total of 335 patients who received TPE between 2010–2021 were retrospectively screened and 59 (male/female, 30/29; min/max-age, 22–84) patients with acute toxic hepatitis who underwent TPE in the first 24 h were included in the study. TPE was performed in patients who had high total bilirubin level (>10 mg/dL). Laboratory parameters of the patients before and after the TPE procedure, number of patients developed complications of acute toxic hepatitis and mortality rates were evaluated for effectiveness of TPE.ResultsAcute toxic hepatitis was associated with hepatotoxic drugs in 44 (74.5 %), herbal medication 6 (10.2 %), mushroom poisoning 6 (10.2 %) and with substance abuse 3 (5.1 %) in patients. When the patients were compared based on INR, liver function tests, ammonia, lactate and Model For End-Stage Liver Disease (MELD) score at baseline, 48 h after TPE (independently of TPE number) and before final state a statistically significant decrease was observed in all parameters (p < 0.05). Fifty three (90 %) of patients improved without complications, the remaining 6 (10 %) patients were diagnosed with fulminant hepatitis. All these remaining patients died before liver transplantation (LTx) could be performed.ConclusionTPE is a safe, tolerable therapy option and early TPE may improve treatment outcomes in severe acute toxic hepatitis.     

In-hospital percentage BNP reduction is highly predictive for adverse events in patients admitted for acute heart failure: the Italian RED Study

Introduction

Our aim was to evaluate the role of B-type natriuretic peptide (BNP) percentage variations at 24 hours and at discharge compared to its value at admission in order to demonstrate its predictive value for outcomes in patients with acute decompensated heart failure (ADHF).

Methods

This was a multicenter Italian (8 centers) observational study (Italian Research Emergency Department: RED). 287 patients with ADHF were studied through physical exams, lab tests, chest X Ray, electrocardiograms (ECGs) and BNP measurements, performed at admission, at 24 hours, and at discharge. Follow up was performed 180 days after hospital discharge. Logistic regression analysis was used to estimate odds ratios (OR) for the various subgroups created. For all comparisons, a P value < 0.05 was considered statistically significant.

Results

BNP median (interquartile range (IQR)) value at admission was 822 (412 - 1390) pg\mL; at 24 hours was 593 (270 - 1953) and at discharge was 325 (160 - 725). A BNP reduction of >46% at discharge had an area under curve (AUC) of 0.70 (P < 0.001) for predicting future adverse events. There were 78 events through follow up and in 58 of these patients the BNP level at discharge was >300 pg/mL. A BNP reduction of 25.9% after 24 hours had an AUC at ROC curve of 0.64 for predicting adverse events (P < 0.001). The odds ratio of the patients whose BNP level at discharge was <300 pg/mL and whose percentage decrease at discharge was <46% compared to the group whose BNP level at discharge was <300 pg/mL and whose percentage decrease at discharge was >46% was 4.775 (95% confidence interval (CI) 1.76 - 12.83, P < 0.002). The odds ratio of the patients whose BNP level at discharge was >300 pg/mL and whose percentage decrease at discharge was <46% compared to the group whose BNP level at discharge was <300 pg/mL and whose percentage decrease at discharge was >46% was 9.614 (CI 4.51 - 20.47, P < 0.001).

Conclusions

A reduction of BNP >46% at hospital discharge compared to the admission levels coupled with a BNP absolute value < 300 pg/mL seems to be a very powerful negative prognostic value for future cardiovascular outcomes in patients hospitalized with ADHF.     

Ethylene Glycol Toxicity: The Role of Serum Glycolic Acid In Hemodialysis

Objective: To correlate serum glycolic acid levels with clinical severity and outcome in ethylene glycol poisoning and to determine if glycolic acid levels are predictive of renal failure and the need for hemodialysis. Methods: We measured serum ethylene glycol and glycolic acid levels by gas chromatography/mass spectrometry for 41 admissions (39 patients) for ethylene glycol ingestion and performed retrospective chart reviews. Results: Eight patients died, all of whom developed acute renal failure. Of the survivors, 15 also developed acute renal failure, whereas 18 did not. Of those with normal renal function, 8 had glycolic acid levels below detection limits (<0.13 mmol/L) despite ethylene glycol levels as high as 710 mg/dL; 7 of these patients coingested ethanol. Pertinent initial laboratory data for each group are as follows (mean; range): Deceased: pH 6.99 (6.82–7.22); bicarbonate, 4.8 mmol/L (2–9); anion gap, 28.6 mmol/L (24–40); glycolic acid, 23.5 mmol/L (13.8–38.0); ethylene glycol, 136.5 mg/dL (6–272). Survived/acute renal failure: pH 7.07 (6.75–7.32); bicarbonate, 5.6 mmol/L (1–12); anion gap, 28.7 mmol/L (18–41); glycolic acid, 20.2 mmol/L (10.0–30.0); ethylene glycol, 238.8 mg/dL (12–810). No acute renal failure with glycolic acid >1.0 mmol/L: pH 7.29 (7.12–7.46); bicarbonate, 14.7 mmol/L (4–23); anion gap, 16.5 mmol/L (10–26); glycolic acid, 6.8 mmol/L (2.6–17.0); ethylene glycol, 269.1 mg/dL (6–675). No acute renal failure with glycolic acid <1.0 mmol/L: pH 7.41 (7.38–7.47); bicarbonate, 23.4 mmol/L (17–25); anion gap, 11.8 mmol/L (8–18); glycolic acid, 0.1 mmol/L (0–0.66); ethylene glycol, 211 mg/dL (8–710). The mean time postingestion to admission generally correlated with severity as follows: deceased, ≥10.4 h; survived/acute renal failure, ≥9.9 h; no acute renal failure with glycolic acid >1.0 mmol/L, ≥6.2 h; no acute renal failure with glycolic acid <1.0 mmol/L, ≥3.7 h. Hematuria was more prevalent than oxaluria (86% and 41%, respectively), but neither was individually predictive of acute renal failure. Good correlations were found between glycolic acid levels and anion gap (r² = 0.7724), pH (r² = 0.7921), and bicarbonate (r² = 0.6579); poor correlations (r² <0.0023) occurred between ethylene glycol levels and glycolic acid, pH, anion gap, and bicarbonate. Measured ethylene glycol values were highly correlated with ethylene glycol values calculated from the osmolal gap (r² = 0.9339), but the latter overestimates the true value by about 7%, on average. An initial glycolic acid level ≥10 mmol/L predicts acute renal failure with a sensitivity of 100%, a specificity of 94.4%, and an efficiency of 97.6%. Ethylene glycol levels are not predictive of acute renal failure or central nervous system manifestations of toxicity. If only ethylene glycol values are available (measured or calculated), an initial anion gap >20 mmol/L is 95.6% sensitive and 94.4% specific for acute renal failure when ethylene glycol is present. Likewise, initial pH <7.30 is 100% sensitive and 88.5% specific for acute renal failure. Conclusion: We propose glycolic acid <8 mmol/L as a criterion for the initiation of hemodialysis in ethylene glycol ingestion. Patients with glycolic acid <8 mmol/L probably do not need dialysis, regardless of the ethylene glycol concentration, when metabolism of ethylene glycol is therapeutically inhibited. In the absence of glycolic acid values, an anion gap >20 mmol/L or pH <7.30 predicts acute renal failure.     

Predictive factors for acute brain lesions on magnetic resonance imaging in acute carbon monoxide poisoning

BackgroundAcute brain lesions on diffusion-weighted-magnetic resonance imaging (MRI) after acute carbon monoxide (CO) poisoning were associated with delayed neurological sequelae. This study was conducted to identify the risk factors associated with acute brain lesions on MRI after acute CO poisoning and to help select patients who need acute-phase brain MRI after acute CO poisoning in the emergency department (ED).MethodsThis retrospective observational study included 103 adult patients who were hospitalized at a tertiary-care hospital between November 2016 and September 2019 and underwent brain MRI because of acute CO poisoning. Multivariable logistic regression analysis was applied to identify predictive factors for acute brain lesions on MRI after acute CO poisoning.ResultsMultivariable logistic regression analysis showed that Glasgow Coma Scale (GCS) score of <9 at ED presentation (odds ratio [OR] 17.749, 95% confidence interval [CI] 3.098–101.690, P = 0.001) and the initial troponin-I level at presentation in the ED (OR 13.657, 95% CI 1.415–131.834, P = 0.024) were predictive factors for acute brain lesions on MRI in acute CO poisoning. The receiver operating characteristics curve for initial troponin-I showed an area under the curve of 0.761 (95% CI 0.638–0.883, P < 0.001) and the optimal cutoff value was 0.105 ng/mL.ConclusionsAcute-phase brain MRI in acute CO poisoning can be considered for patients who present at the ED with a GCS score <9 or troponin-I level >0.105 ng/mL.     

Biochemical features in patients with their first acute inferior myocardial infarction

Summary. Sixty eight patients with their first acute inferior myocardial infarction were studied within 24 h of the onset of chest pain by vectorcardiography and biochemical indicators. Patients were divided into three groups according to the vectorcardiographic findings: Group 1 (31 patients with inferior myocardial infarction); Group 2 (26 patients with inferior myocardial infarction and right ventricular involvement); and Group 3 (11 patients with inferior-posterior infarction). Biochemical studies showed that the tendency for the magnitude of enzyme release varied with the site inferior-posterior > inferior + right ventricular > inferior groups. However, the differences between inferior and inferior plus right-ventricular groups were not significant. This suggests that the left ventricle dominates enzyme release regardless, with or without right ventricular involvement in patients with acute inferior myocardial infarction. When the enzyme levels in inferior and inferior-posterior myocardial infarction are compared, the HBDH and CK-MB were significantly higher (2 P < 0–02 and 2 P < 0–05 respectively). This confirms that when the vectorcardiographic QRS loop changes are large, more enzyme is released during acute myocardial infarction.,