Survival of acute hypernatremia due to massive soy sauce ingestion.

BACKGROUND: Intentional massive sodium chloride ingestions are rare occurrences and are often fatal. OBJECTIVES: There are a variety of treatment recommendations for hypernatremia, ranging from dialysis to varying rates of correction. We report a case of acute severe hypernatremia corrected with rapid free-water infusions that, to our knowledge, has not been previously reported. CASE REPORT: A 19-year-old man presented to the Emergency Department in a comatose state with seizure-like activity 2 hours after ingesting a quart of soy sauce. He was administered 6 L of free water over 30 min and survived neurologically intact without clinical sequelae. Corrected for hyperglycemia, the patient's peak serum sodium was 196 mmol/L, which, to our knowledge, is the highest documented level in an adult patient to survive an acute sodium ingestion without neurologic deficits. CONCLUSION: Emergency physicians should consider rapidly lowering serum sodium with hypotonic intravenous fluids as a potential management strategy for acute severe hypernatremia secondary to massive salt ingestion.

Ruptured heterotopic pregnancy presenting with relative bradycardia in a woman not receiving reproductive assistance.

We report a case of heterotopic pregnancy in a woman who had not undergone in vitro fertilization or any other reproductive assistance. The patient failed to mount a tachycardic response to hemorrhagic shock. Bradycardia is a well-established phenomenon in the setting of hemoperitoneum and particularly with ruptured ectopic pregnancy. This is a case of heterotopic pregnancy with relative bradycardia in a woman without predisposing factors for heterotopic pregnancy. We make suggestions on avoiding common pitfalls in the emergency department diagnosis of heterotopic pregnancy. We also address the similar clinical presentations of heterotopic pregnancy and intrauterine pregnancy with ruptured corpus luteum cyst.

Electrocardiographic ST segment elevation: a comparison of AMI and non-AMI ECG syndromes.

Chest pain (CP) patients presenting to the ED may manifest electrocardiographic ST segment elevation (STE). AMI (acute myocardial infarction) is a less frequent cause of such abnormality and one of many patterns responsible for ST segment elevation in ED CP patients. We performed a retrospective comparative review of the electrocardiographic features of various STE syndromes, focusing on differences between AMI and non-AMI syndromes. The electrocardiograms (ECGs) of consecutive ED adult CP patients (with 3 serial troponin I determinations) were interpreted by 3 attending emergency physicians. These ECGs with STE represented the study population used for analysis. Various electrocardiographic features such as STE, ST segment depression (STD), STE morphology, anatomic distribution of STE, and the number of leads with STE were recorded; derived values such as total STE, total ST segment deviation, and average STE per lead were calculated. Interobserver reliability concerning STE morphology was determined. AMI was diagnosed by abnormal serum troponin I values (>0.1 mg/dL) followed by a rise and fall of the serum marker; STE diagnoses of non-AMI causes were determined by medical record review. Five hundred ninety-nine CP patients were entered in the study with 212 (35%) individuals showing STE, 55 (26%) with electrocardiographic AMI and 157 (74%) with non-AMI electrocardiographic syndromes. Anatomic location within the AMI group included 32 inferior and inferior variants, 18 anterior and anterior variants, and 5 lateral; non-AMI anatomic locations included 56 inferior and inferior variants, 98 anterior and anterior variants, and 3 lateral; anterior STE occurred significantly more often in non-AMI syndromes. Total STE was 15.3 mm in AMI patients and 7.4 mm in non-AMI patients (P =.0004). The number of leads with STE was not significantly different between the two groups, 3.4 mm in AMI and 4.1 in non-AMI syndromes. ST segment elevation per lead was not significantly different in the 2 groups, 4.4 mm in AMI versus 1.8 mm in non-AMI syndromes. Total ST segment deviation (sum of STE and STD) was significantly greater in AMI syndromes, 17.8 mm in AMI compared with 10.5 mm in non-AMI syndromes (P =.00009). The presence of STD occurred at statistically similar rates in both groups. The morphology of the STE occurred in significantly different rates between AMI and non-AMI patterns, concave more often in non-AMI patterns (P <.00001) and nonconcave more often in AMI (P <.00001). Non-AMI causes of STE account for the majority of electrocardiographic syndromes encountered in ED chest pain patients. These findings alone are not adequate to determine the electrocardiographic cause of the ST segment elevation in chest pain patients. When determining AMI versus non-AMI with the ECG, these various findings should be used in the consideration of the overall clinical picture (history, examination, and electrocardiogram) in chest pain patients with ST segment elevation.

Reciprocal ST segment depression: impact on the electrocardiographic diagnosis of ST segment elevation acute myocardial infarction.

Acute myocardial infarction (AMI) is one of many causes of electrocardiographic ST segment elevation (STE) in ED chest pain (CP) patients; at times, the electrocardiographic diagnosis may be difficult. Coexistent ST segment depression has been reported to assist in the differentiation of non-infarction causes of STE from AMI-related ST segment elevation. The objective was to determine the effect of AMI diagnosis on the presence of STD among ED CP patients with electrocardiographic STE. Adult CP patients with electrocardiographic STE in at least 2 anatomically distributed leads were reviewed for the presence or absence of ST segment depression in at least 1 lead and separated into 2 groups, both with and without ST segment depression. A comparison of the 2 groups was performed in 2 approaches: all STE patients and then only with STE patients who lacked confounding electrocardiographic pattern (bundle branch block [BBB], left ventricular hypertrophy [LVH], or right ventricular paced rhythm [VPR]). All patients in the study underwent prolonged observation in the ED (at least 8 hours) with 3 serial troponin T determinations and 3 electrocardiograms (ECG). AMI was diagnosed by abnormal serum troponin T values (>0.1 mg/dL); electrocardiographic STE diagnoses of non-AMI causes were determined by medical record review. There were 171 CP patients with STE were entered in the study with 112 (65.5%) individuals show ST segment depression. When considering all study patients, ST segment depression was present at statistically equal rates in AMI and non-AMI situations (P = NS). The sensitivity, specificity, positive predictive value, and negative predictive value for the electrocardiographic diagnosis of AMI were 63%, 34%, 30%, and 67%, respectively. Patients with confounding patterns (LVH 46, BBB 19, and VPR 6) were removed from the analysis group, leaving 100 patients for analysis; 38 of these patients had ST segment depression. When considering this group of study patients, ST segment depression was present significantly more often in AMI patients (P <.0001). The sensitivity, specificity, positive predictive value, and negative predictive value for the electrocardiographic diagnosis of AMI were 69%, 93%, 93%, and 71%, respectively. Clinical diagnoses were as follows: 56 AMI, 50 USAP, and 65 noncoronary syndrome. When all CP patients with electrocardiographic STE are considered, the presence of ST segment depression is not helpful in distinguishing AMI from non-AMI. If one considers only patterns which lack electrocardiographic ST segment depression caused by altered intraventricular conduction, the presence of ST segment depression strongly suggests the diagnosis of AMI. In these cases, reciprocal ST segment depression is of considerable value in establishing the electrocardiographic diagnosis of STE AMI.