Synthetic Phenylpiperidine Derivative Meperidine as a Trigger for Type I Negative Pressure Pulmonary Edema in General Anesthesia

Abstract

We present a case of type I negative pressure pulmonary edema in a healthy 17-year-old boy who underwent an emergent appendectomy under general anesthesia. The particularity of our case revolves around the administration of meperidine for perioperative shivering, along with other anesthetic risk factors, which may have served as the trigger of type I negative pressure pulmonary edema.We present the pathophysiological mechanisms, the formulation of clinical and paraclinical diagnosis and the principles of intensive care therapy. This was the first such case experienced in our practice, with a remarkable learning opportunity.Negative pressure pulmonary edema (NPPE) is an acute, potentially life threatening, uncommon perioperative pathological entity. Two clinical types have been described: type I NPPE, associated with acute airway obstruction, and type II NPPE, associated with chronic partial upper airway obstruction. An early differential diagnosis between various pulmonary edema conditions in critically ill patients and a prompt recognition of high risk of acute morbidity are crucial in certain circumstances. We present a case of type I NPPE in a healthy 17-year-old boy who underwent an emergent appendectomy under general anesthesia. The particularity of our case revolves around the administration of meperidine, along with other anesthetic risk factors, which may have served as the trigger of NPPE. Experimental part Study case presentationA 17-year-old male patient without medical history presented with acute appendicitis. After evaluation in the emergency department, he was admitted for emergency appendectomy. His preoperative physical examination and laboratory tests were within normal limits except for neutrophilic leukocytosis.Physical status: height (H) = 1.60 m; weight (W) = 50 kg; body mass index (BMI) = 19.53 kg/m 2 ; airway assessment by Mallampati classification of oral opening -Mallampati I.Cardiovascular status: blood pressure (BP) = 117/59 mmHg; heart rate (HR) = 75 bpm; heart auscultationnormal.Respiratory status: chest auscultation was clear bilaterally, without murmurs. His baseline pulse oximetry arterial blood oxygen saturation (SpO 2 ) was 99% on room air, with a fraction of inspired oxygen (FiO 2 ) of 0.21. * email: claudiagavris@yahoo.com, Phone: +40723791322; vlader2000@yahoo.com, Phone: +40723271972 Laboratory blood investigations: hemoglobin (Hgb) = 15.2 g/L; hematocrit (Hct) = 42%; leukocytes (L) = 9,450/ µL (neutrophils = 90%); platelets (PLT) = 221,000/µL; activated partial prothrombine time (aPTT) = 24.4 s; international normalized ratio (INR) = 1.09; serum proteins = 71 g/L; fibrinogen = 3.22 g/L; C-reactive protein (CRP) = 11.3 mg/L; glycemia = 110 mg/dL; serum Na + = 135 mmol/L; serum K + = 4.1 mmol/L; serum Cl -= 98,5 mmol/ L; serum total calcium = 9.43 mg/dL; serum Mg + = 1.81 mg/dL; aspartate aminotrasferase (AST) = 20 U/L; alanine aminotransferase (ALT) = 18 U/L; lactate dehidrogenase (LDH) = 374 U/L; blood urea nitrogen (BUN) = 33.3 mg/ dL; creatinine = 1.06 mg/dL.The patient w...

Nosocomial Infections Distribution and Impact in Medical Units

“…So, it is precisely the patients who benefit today more from the quality of care who are the most vulnerable, which paradoxically causes a decrease in their chance of survival by exposure to infectious complications. In this situation, only discipline and strict supervision of hygiene rules in hospitals can control nosocomial infections and, ultimately, the chance of survival of these patients [9][10][11][12].…”