The utility of routine laboratory testing in hypoglycaemic emergency department patients.

BACKGROUND: After treating a hypoglycaemic patient, how in-depth a work-up is required to prevent their next hypoglycaemic episode? OBJECTIVE: To determine the utility of routine laboratory testing in the management of hypoglycaemia. METHODS: A cross-sectional study at two urban teaching hospitals from July 2006 to July 2007. The study included adult patients (> or = 18 years) with hypoglycaemia (fingerstick glucose < or = 60 mg/dl (3.33 mmol/l) in the emergency department or altered mental status resolved by glucose or glucagon). Predictor variables were age, gender, medical history, physical examination, hypoglycaemic agent (insulin vs oral hypoglycaemic). Outcome variables were electrolyte abnormality (serum sodium outside the range of 135-145 mmol/l; serum potassium outside the range of 3.5-5.0 mEq/dl), leucocytosis (white blood cell count >15,000/high power field) or urinary tract infection. Continuous data are presented as mean (SD). Categorical data are presented as percentages with 95% confidence intervals. Student's t and Fisher's exact tests were used to compare data when appropriate (alpha = 0.05, two-tailed). RESULTS: 291 patients were studied with a mean age of 64 years (SD 16) (range 22-95) 54 women. 200 patients (69%, 95% CI 63% to 74%) had at least one laboratory abnormality. These included newly diagnosed renal failure (23%), pre-existing renal failure (32%), hypokalaemia (8%), hyperkalaemia (11%), leucocytosis (4.2%) and pyuria (19%). No significant difference was found between the rates of abnormal laboratory results in patients on insulin versus those on oral hypoglycaemics. Higher admission rates (p = 0.001) were also observed in patients with abnormal (70%) compared with normal (53%) laboratory results. CONCLUSION: The high rate of laboratory abnormalities in hypoglycaemic patients justifies routine testing.

Serum ionized magnesium and calcium levels in adult patients with seizures.

OBJECTIVE: Prior studies have been equivocal about whether or not serum levels of the divalent ions calcium and magnesium are altered during different types of seizures. Magnesium is a potential modulator of seizure activity because of its ability to antagonize the excitatory calcium influx through the N-methyl-D-aspartate (NMDA) receptor. We hypothesize that serum ionized levels of calcium (Ca(2+)) and magnesium (Mg(2+)) would be altered significantly during certain types of seizures. MATERIAL AND METHODS: A convenience sample of seizure patients presenting to an emergency department (ED) were enrolled in this prospective study. Novel ion-selective electrodes were used to measure Ca(2+) and Mg(2+). Data were reported as mean values+/-standard deviations. Group comparisons were analyzed by ANOVA with post-hoc testing using the Bonferroni, or the Fisher exact test, where appropriate, alpha = 0.05 (two-tailed). RESULTS: Forty-nine patients with seizure and 32 healthy racially matched controls were included in the study. Seizure patients had a significantly (p<0.001) lower mean Mg(2+), but not total serum Mg and a significantly (p<0.001) higher Ca(2+)/Mg(2+) ratio than that in controls. CONCLUSIONS: We were able to show significantly lower Mg(2+) and higher ionized Ca(2+)/Mg(2+) ratios in seizure patients compared with a racially matched control group.

Ionized magnesium levels and the ratio of ionized calcium to magnesium in asthma patients before and after treatment with magnesium.

OBJECTIVE: Prior studies have been equivocal about the efficacy of magnesium therapy in acute asthma exacerbations. We hypothesize that pretreatment ionized magnesium (Mg(2+)) levels and/or the ratio of ionized calcium to ionized magnesium (Ca(2+)/Mg(2+)) may have been confounding variables in these previous studies. Here, we report on the incidence of abnormal divalent ion levels in our asthma population. MATERIAL AND METHODS: The study was designed as a randomized, double-blind, placebo-controlled trial of intravenous magnesium. Inclusion criteria were: age >18 years, percentage predicted forced expiratory volume (FEV(1)) <75 % after an initial beta-agonist. African-American patients (AA) at an urban university hospital were randomized to 2 g IV Mg or placebo. Mg(2+) and Ca(2+)/Mg(2+) levels were measured pre- and post-infusion. Data were reported as means+/-SD. Student's t-test and Fisher's exact test were used where appropriate (alpha = 0.05, two tailed). RESULTS: Fifty-five AA patients (mean age of 42.7 years+/-15.6 years, range 18-75 years) were studied. A significantly (p<0.05) lower level of Mg(2+) was found in asthma (AS) patients compared with that in the AA group, by 0.03 mmol/L (95 % CI, 0.007-0.053 mmol/L). The AS group had a mean increase in Ca(2+)/Mg(2+) ratios over the AA group, of 0.27 (95 % CI, 0.16-0.38); 100 % of patients with abnormal divalent ion levels were corrected with IV magnesium. CONCLUSIONS: We identified a subgroup of asthmatic patients with significant abnormalities in their divalent ion concentrations, which was corrected with IV magnesium.

The effect of pregnancy on the response to blood loss in a rat model.

STUDY OBJECTIVES: A commonly held belief is that the blunted hemodynamic response to hemorrhage observed in pregnant women is secondary to expanded blood volume. In addition to increased blood volume, pregnancy is also a vasodilated state. Vasodilatation may have deleterious effects on the response to hemorrhage by inhibiting central blood shunting after blood loss. How these conflicting variables of increased blood volume and vasodilatation integrate into a whole body model of maternal hemorrhagic shock has yet to be studied in a controlled experiment. We tested the null hypothesis that there would be no difference in the hemodynamic and metabolic responses to hemorrhage between pregnant (PRG) and non-pregnant (NPRG) rats. METHODS: Twenty-four adult female Sprague-Dawley rats (12 PRG and 12 NPRG) were anesthetized with Althesin via the intraperitoneal route. Femoral arteries were cannulated by cut-down. Twelve (six PRG and six NPRG) rats underwent controlled catheter hemorrhage of 25% of their total blood volume. Twelve rats (six PRG and six NPRG) served as non-hemorrhage controls. Mean arterial pressure (MAP) and base excess (BE) were measured pre-hemorrhage and then every 15 min post-hemorrhage for the next 90 min. Data were reported as mean+/-standard error of the mean (S.E.M.) over the 90-min post-hemorrhage observation period. Group comparisons were analyzed by ANOVA with repeated values post-hoc by Bonferroni. Statistical significance was defined by an alpha=0.05. RESULTS: PRG and NPRG rats were evenly matched for MAP (P=0.788) and BE (P=0.146) pre-hemorrhage. Post-hemorrhage there were no mortalities in either group. Post-hemorrhage both the PRG and NPRG groups experienced significant (P=0.011) drops in systolic and diastolic blood pressures as compared to their non-hemorrhage controls. Post-hemorrhage there was no significant (P=0.43) difference in MAP between the PRG (89+/-2 mmHg) and NPRG (80+/-2 mmHg) rats. BE also dropped significantly within both PRG (P=0.004) and NPRG (P=0.001) groups post-hemorrhage. No significant (P=0.672) difference was noted in BE between PRG and NPRG groups post-hemorrhage -6.1+/-0.3 mEq/l and -6.9+/-0.4 mEq/l, respectively. CONCLUSION: After a controlled hemorrhage of 25% of total blood volume we found no significant differences in MAP and BE between pregnant and non-pregnant rats. Pregnancy does not affect the response to hemorrhage.

The effect of hypertension on the response to blood loss in a rodent model.

OBJECTIVE: Hypertensive patients having higher baseline peripheral resistance and sympathetic tone than normotensive patients may have aberrant responses to hemorrhage. In an attempt to further characterize this clinical observation, the authors compared the hemodynamic and metabolic responses to hemorrhage between spontaneously hypertensive rats (SHR) and normotensive rats (NTR). METHODS: Twenty adult rats (10 NTR and 10 SHR) were anesthetized with althesin via the intraperitoneal route. Femoral arteries were cannulated by cutdown. Twelve (6 SHR and 6 NTR) rats underwent controlled catheter hemorrhage of 25% of their total blood volumes. Eight rats (4 SHR and 4 NTR) served as nonhemorrhage controls. Mean arterial pressure (MAP) and base excess (BE) were measured prehemorrhage and then every 15 minutes for the next 120 minutes. Data were reported as mean +/- standard error of the mean (SEM). Group comparisons were analyzed by ANOVA with repeated values post-hoc by Bonferroni. Statistical significance was defined by an alpha = 0.05. RESULTS: Immediately after hemorrhage, the SHR group experienced a significantly (p < 0.001) greater drop in MAP of 70 +/- 4% in the SHR vs 40 +/- 6% in the NTR. Blood pressure in the NTR returned to control values 15 minutes after hemorrhage, but the SHR remained relatively hypotensive for the entire length of the experiment. Base excess in the SHR decreased significantly (p < 0.004) by 8.2 +/- 2 mmol/L from control values, as compared with no changes in BE for the NTR. CONCLUSIONS: The authors observed significant differences in the response to hemorrhage between hypertensive and normotensive rats. Hypertensive rats experienced a more profound hemorrhagic shock insult than normotensives for the same degree of blood loss.

A successful effort to improve asthma care outcome in an inner-city emergency department.

The purpose of this study was to improve asthma care and outcome in an inner-city emergency department. Consecutive adult patients (19,802) presenting with the diagnosis of acute asthma exacerbation to an inner-city municipal hospital emergency department, between July 1991 and December 1993, were prospectively evaluated. These patients were compared to a historical control group of 7923 consecutive asthma emergency department patients presenting in the year prior to our intervention. An asthma treatment guideline was implemented through a continuous quality improvement process. Asthma relapse rate and admission rate were obtained before and after the guidelines were instituted. Data after interventions were also prospectively compared to asthma outcomes at all other New York City municipal hospital emergency departments. After intervention, mean monthly asthma relapse rates showed a significant reduction from 12.18% to 7.83% (p < 0.001). A similar decrease was also noted in the monthly asthma admission rate, from 4.85 to 3.90 per 100 emergency department visits (p < 0.05). Asthma treatment guidelines along with continuous quality improvement techniques can significantly improve the outcome of inner-city emergency department asthma patients.

Effects of traditional versus delayed resuscitation on serum lactate and base deficit.

OBJECTIVE: To test the hypothesis that delayed resuscitation of hemorrhagic shock produces a less severe shock insult than traditional resuscitation, characterized by repeated episodes of alternating hypotension and normotension. METHODS: Female pigs were divided into three groups. Sham operated controls (C) (n = 4), sustained hypotension (SS) (n = 6), and hypotension with multiple cycles of shock and resuscitation (SR) (n = 6). SS and SR animals were bled to a mean arterial pressure (MAP) of 50 mmHg. SS animals were maintained at an MAP of 50 mmHg for 65 min and then resuscitated to baseline blood pressure with normal saline and shed blood. SR animals were initially bled and maintained at an MAP of 50 mmHg for 35 min, resuscitated to baseline BP, and subsequently bled and resuscitated twice more. The total period of shock was the same in both SS and SR. RESULTS: Following hemorrhage, there was a significant increase in lactate and base deficit in SS as compared to C and SR. CONCLUSION: Delayed resuscitation produces a more profound shock insult than traditional resuscitation.

Management of nontraumatic subarachnoid hemorrhage in a patient with sickle-cell disease: a case report.

Subarachnoid hemorrhage (SAH) due to sickle-cell anemia is rare, but potentially devastating. However, with early recognition of SAH, aggressive support with exchange transfusion, cerebral angiography, and neurosurgical intervention, a positive outcome may be achieved. A case report of SAH managed in this fashion is reported. Based on similar cases in the literature, a suggested treatment protocol is provided for the management of nontraumatic SAH in sickle-cell patients presenting to the ED.

The efficacy of erythropoietin in human immunodeficiency virus-infected end-stage renal disease patients treated by maintenance hemodialysis.

The superimposition of human immunodeficiency virus (HIV) infection, associated opportunistic infections, and anti-retroviral therapy further worsens the severity of anemia in patients also suffering from end-stage renal disease. A major cause of anemia in renal failure is a deficiency of erythropoietin. The causes of anemia in HIV disease include direct and indirect stem cell inhibition by the virus, increased peripheral destruction of red blood cells, and bone marrow suppression by various opportunistic infections and therapeutic drugs, particularly zidovudine. We compared the efficacy of recombinant human erythropoietin (rHuEPO) therapy in improving the anemia in HIV-infected end-stage renal disease patients (group I) with that in nondiabetic (group II) and diabetic (group III) hemodialysis patients without HIV infection. All three groups of patients were comparable in dialysis prescription and serum iron studies. Iron supplementation was prescribed to all patients, and none received blood transfusions. After 8 weeks of rHuEPO therapy (administered intravenously in a dose of 100 U/kg body weight thrice weekly), the mean increase in hematocrit was similar in all responders (5.8% increase in hematocrit in 23 of 30 HIV patients and 6.7% increase in 24 of 30 non-HIV patients). Response in hematocrit was noted in HIV patients despite the presence of opportunistic infections in 15 and zidovudine administration in 11. Seven HIV-positive patients and six non-HIV patients failed to respond to rHuEPO. Irrespective of the HIV status, the baseline serum EPO levels in patients responding to rHuEPO were significantly lower than those in nonresponders.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute isoniazid neurotoxicity in an urban hospital.

OBJECTIVES: To describe the presentation and treatment of acute isoniazid (INH) neurotoxicity appearing at an inner-city municipal hospital. DESIGN: Case series. PARTICIPANTS: Seven patients (eight patient visits) with an age range of 5 days to 14.9 years. RESULTS: At our institution, no children appeared with acute INH neurotoxicity in the period 1985 through 1990, whereas seven patients were treated from 1991 through 1993. This paralleled the rise in the number of children with tuberculous infection and disease seen at our institution, from an average 96 per year to 213 per year during these two time periods. All seven patients were receiving INH daily for tuberculosis (TB) prophylaxis. Accidental ingestion (five episodes) and suicidal attempts (three episodes) accounted for these visits. The total amount ingested range from 14.3 to 99.3 mg/kg (mean, 54 mg/kg). All but one patient presented with afebrile seizures. One patient presented twice with seizures. Acute INH neurotoxicity was not suspected on the first admission; however, when readmitted 4 weeks later with another seizure, the diagnosis of acute INH neurotoxicity was made. INTERVENTION: Intravenous pyridoxine was used in five episodes. Because it was not a stocked item in our pediatric emergency cart (as well as at another hospital, necessitating a transfer of a patient with refractory seizures to our hospital), the average delay was 5.8 hours (range, 1.3 to 13 hours) before it was given. Two patients with refractory seizures failed to respond to anticonvulsants, and their seizures were controlled only after parenteral pyridoxine. CONCLUSIONS: We have seen an increased incidence of acute INH neurotoxicity because of the resurgence of TB in New York City. Others as well may see a similar rise based on local trends in TB infection and disease. Acute INH toxicity should be suspected in children presenting with seizures with or without fever. In patients with a known access to INH, seizures should be considered to be caused by INH toxicity unless proved otherwise. Parenteral pyridoxine, the specific antidote for INH-induced refractory seizures, should be readily available in every emergency department in the areas similarly experiencing increasing trends of TB.

Percutaneous central venous access for resuscitation in trauma.

OBJECTIVE: To determine the safety of percutaneous central venous access when used for trauma resuscitation and whether the initial hemodynamic status of the patient or the site of placement affects the ease or success of line placement. METHOD: Consecutive major-trauma patients were managed using a resuscitation protocol guiding intravenous line use. Percutaneous peripheral venous access was initially attempted in all patients. If this approach was unsuccessful or proved to be inadequate for volume resuscitation, venous access was attempted using central venous catheter-introducer sets. The site of the central venous access was determined by protocol. For thoracic injury, access was via the ipsilateral subclavian vein (SCV), the ipsilateral internal jugular vein (IJV), or the femoral vein. For suspected mediastinal injury, access was via the contralateral SCV or IJV, or the femoral vein. For abdominal or flank injury, access was via the SCV or IJV only. Multiple central venous access sites were used at the discretion of the trauma team. RESULTS: Central venous access was successful at 144 of 147 sites (99%) used in 122 patients during the study period. There was only one major complication (rate = 0.7%; 95% CI 0.0-3.8%). Mean catheter placement time was 1.9 minutes, and cannulation occurred with a mean of 1.8 needle passes. Most patients (81/122) were hypotensive (blood pressure < or = 90 torr) at the time of line placement, including 44 who were in cardiac arrest and four awake patients who had no obtainable blood pressure. Neither the access site nor the presence of hypotension was associated with the mean time to obtain central venous access, the mean number of attempts, or the complication rate. CONCLUSION: Percutaneous central venous access is relatively safe and reliable for gaining intravenous access when resuscitating trauma patients, when used in a center where physicians are experienced in the technique. Consideration should be given to expanding the use of central venous access in trauma resuscitation.

Exercise-induced rhabdomyolysis.

STUDY OBJECTIVE: To describe the syndrome of exercise-induced rhabdomyolysis and to investigate the relation between exercise-induced rhabdomyolysis and the development of acute renal failure. DESIGN: Retrospective chart analysis on all patients with a discharge diagnosis of rhabdomyolysis from January 1988 to January 1993. SETTING: An urban tertiary care center with 225,000 annual emergency department visits. TYPE OF PARTICIPANTS: Thirty-five patients met the inclusion criteria for exercise-induced rhabdomyolysis: a history of strenuous exercise, creatine phosphokinase level more than 500, and urine dipstick positive for blood without hematuria. We excluded patients with a history of trauma, myocardial infarction, stroke, or documented sepsis. Charts also were examined for the presence of nephrotoxic cofactors (ie, hypovolemia and/or acidosis). RESULTS: All 35 patients were men without significant past medical history and were an average age of 24.4 years. The average admission creatine phosphokinase was 40,471 U/L. No patient presented with or developed nephrotoxic cofactors during hospitalization. None of our study patients experienced acute renal failure. CONCLUSION: Previous literature has described a 17% to 40% incidence of acute renal failure in rhabdomyolysis. None of our patients developed acute renal failure, signifying a much lower incidence of acute renal failure in exercise-induced rhabdomyolysis without nephrotoxic cofactors than in other forms of rhabdomyolysis.

Retropharyngeal and bowel hematomas in an anticoagulated patient.

As the indications for oral anticoagulation therapy increase, the number of patients being treated with anticoagulants and at risk for complications also will rise. Major bleeding episodes have been reported to occur in approximately 2-4% of patients being treated with oral anticoagulants. The case report of a patient with concurrent spontaneous retropharyngeal and small-bowel hematomas from overanticoagulation with warfarin is presented. The authors review the subtle presentation of retropharyngeal hematomas, common medications that may enhance warfarin anticoagulation, and therapy of potentially life-threatening hematomas. Airway management and possible surgical therapies to treat the complications of hematomas are discussed. Depending upon the indication for the initial anticoagulation, interim anticoagulation with heparin may be indicated.

Modulation of ionic permeability in a nonpolarized cell: effect of cAMP.

To evaluate whether adenosine 3',5'-cyclic monophosphate (cAMP) modulates ionic permeabilities of nonpolarized cells, as reported in diverse polarized epithelia, relative ionic permeabilities were determined in human red cell ghosts by means of the potential-sensitive fluorescent probe 3,3'-dipropylthiadicarbocyanine iodide. Relative ionic chloride permeability (PCl/PK), but not PNa/PK, was significantly increased in ghosts prepared from normal red blood cells (RBCs) exposed to cAMP analogues or forskolin, with the latter at a concentration that significantly increased intracellular cAMP concentration. As basal RBC cAMP concentrations of untreated uremic subjects were also increased, relative permeabilities of ghosts and unstimulated RBC cAMP concentrations were compared in normal, uremic, and dialyzed subjects, PCl/PK was significantly increased in uremic compared with normal subjects; PNa/PK was not altered. PCl/PK and RBC cAMP concentrations were indistinguishable in normal and dialyzed subjects. Neither the kinetics nor number of Cl(-)-HCO3- antiporters, assessed with the pH-sensitive probe acridine orange and the disulfonic stilbene 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, respectively, were altered in uremic cells. These studies suggest that cAMP modulates ionic chloride permeability via increased chloride conductance of each Cl(-)-HCO3- antiporter or by activation/opening of new or existing channels in RBC membranes.