Role of clinical suspicion in pediatric blunt trauma patients with severe mechanisms of injury

Objectives

In adult patients with blunt trauma, severe mechanism of injury leads to routine pan-computed tomography (CT). Due to concerns about the risk of radiation, we sought to determine whether clinical suspicion could identify children requiring radiographic imaging.

Chest pain as a manifestation of hypokalemia in a pediatric patient

Patients presenting to the emergency department with chest pain are common and a cause of significant concern to patients and families and physicians alike. The causes of chest pain are myriad. These causes span diverse categories including cardiovascular, respiratory, abdominal and gastrointestinal, musculoskeletal, psychiatric, hematologic and oncologic, and neurologic Thull-Freedman (2010) [1]. These diverse etiologies present a diagnostic and management challenge to the ER physician who is tasked to minimize unnecessary diagnostics while not missing any significant disease. Multiple reviews have discussed the various etiologies of chest pain in the pediatric patient presenting to the ER but none of these recent reviews has included hypokalemia as a cause of chest pain Talner and Carboni (2000), Cava and Sayger (2004), Ringstrom and Freedman (2006), Foy and Filippone (2015), Yeh and Yeh (2015) [2], [3], [4], [5], [6]. Additionally, no reviews of hypokalemia describe this condition presenting with chest pain (Mandal, 1997; Gennari, 2002; Medford-Davis and Rafique, 2014 [7], [8], [9]).This case report describes a pediatric patient who presents with chest pain that was attributed to hypokalemia. This report attempts to make practitioners aware that hypokalemia may present with chest pain and to encourage ER providers to include this in the differential diagnosis.     

Modulation of human neutrophil chemotactic responses by cyclic 3',5'-guanosine monophosphate and cyclic 3',5'-adenosine monophosphate.

Cyclic 3',5'-guanosine monophosphate (cGMP) and cyclic 3',5'-adenosine monophosphate (cAMP) and compounds known to effect the intracellular concentrations of these nucleotides were examined for their ability to effect human neutrophil (PMN) responsiveness to chemotactic stimulation. Incubation of neutrophils with agents recognized to promote increases in intracellular cAMP in a variety of tissues (i.e., epinephrine, norepinephrine, isoproterenol, histamine, cholera toxin, and prostaglandin E-1 and E-2) or with cAMP inhibited the leukotactic response to a bacterial chemotactic factor. In contrast, cGMP and compounds which have been shown to promote increases in intracellular cGMP concentration (i.e., acetylcholine, carbamylcholine, phorbol myristate acetate, and prostaglindin F-2-alpha) markedly enhanced the neutrophil chemotactic response. The inhibitory or stimulatory influences on chemotactic responsiveness promoted by several of the agents could be shown to be blocked by a specific pharmacologic antagonist of the particular compound tested. These data support the hypothesis that cGMP and cAMP can provide opposing regulatory influences on certain cellular functions; in this case, directed motility of leukocytes.     

Placental transfer of aspartate and its metabolites in the primate.

The placental transfer of aspartate was tested in pregnant monkeys infused maternally with sodium aspartate. In five animals infused at 100 mg/kg/hr, maternal plasma aspartate levels increased from 0.36 ± 0.19 to 80.2 ± 11.5 μmole/dl (mean ± SD). However, fetal plasma aspartate levels increased only slightly from 0.42 ± 0.31 to 0.98 ± 0.24 μmole/dl (p = 0.02). Erythrocyte aspartate levels were unchanged in both fetal and maternal circulation. In two animals infused at 200 mg/kg/hr, maternal plasma aspartate levels increased from 0.28 and 0.31 μmole/dl to values of 141 and 237 μmole/dl, respectively. This increase produced a significant (p = 0.001) increase in fetal plasma aspartate levels from 0.53 and 0.67 to 3.3 and 4.5 μmole/dl, respectively. Maternal plasma aspartate levels in two animals infused at 400 mg/kg/hr increased from 0.5 and 0.7 μmole/dl to 400 and 750 μmole/dl, respectively, at the end of the infusion. Fetal plasma aspartate levels increased from 0.21 and 0.25 μmole/dl to 60 and 92 μmole/dl, respectively. Maternal aspartate infusion at each level increased maternal, but not fetal, plasma taurine levels. The increase in maternal taurine levels was not in proportion to the dose of aspartate infused. Aspartate metabolites, glucose, and lactate were readily transferred across the placenta. The data indicate that aspartate, like glutamate but unlike most amino acids, is not concentrated toward the fetal circulation in the pregnant primate, and suggest that a barrier to aspartate transfer exists unless maternal plasma levels are grossly elevated.     

Noninvasive Methods for Determining Pulmonary Vascular Function in Children with Pulmonary Arterial Hypertension: Application of a Mechanical Oscillator Model

Objective. Noninvasive diagnostics for pulmonary arterial hypertension (PAH) have traditionally sought to predict main pulmonary artery pressure from qualitative or direct quantitative measures of the flow velocity pattern obtained from spectral Doppler ultrasound examination of the main pulmonary artery. A more detailed quantification of flow velocity patterns in the systemic circuit has been obtained by parameterizing the flow trace with a simple dynamic system model. Here, we investigate such a model's utility as a noninvasive predictor of total right heart afterload and right heart function. Design. Flow velocity and pressure was measured within the main pulmonary artery during right heart catheterization of patients with normal hemodynamics (19 subjects, 20 conditions) and those with PAH undergoing reactivity evaluation (34 patients, 69 conditions). Our model parameters were obtained by least‐squares fitting the model velocity to the measured flow velocity. Results. Five parameter means displayed significant (P < .05) differences between normotensive and hypertensive groups. The model stiffness parameter correlated to actual pulmonary vascular resistance (r = 0.4924), pulmonary vascular stiffness (r = 0.6811), pulmonary flow (r = 0.6963), and stroke work (r = 0.7017), while the model initial displacement parameter had good correlation to stiffness (r = 0.6943) and flow (r = 0.6958). Conclusions. As predictors of total right heart afterload (resistance and stiffness) and right ventricle work, the model parameters of stiffness and initial displacement offer more comprehensive measures of the disease state than previous noninvasive methods and may be useful in routine diagnostic monitoring of patients with PAH.