Bronchopulmonary dysplasia (BPD) is a chronic lung disease most commonly seen in preterm infants of low birthweight who required postnatal respiratory support. Although overall incidence rates have not changed, recent advancements in medical care have resulted in lower mortality rates, and those affected are beginning to live longer. As a result, the long-term repercussions of BPD are becoming more apparent. Whereas BPD has been thought of as a disease of just the lungs, resulting in abnormalities such as increased susceptibility to pulmonary infections, impaired exercise tolerance, and pulmonary hypertension, the enduring complications of BPD have been found to extend much further. This includes an increased risk for cerebral palsy and developmental delays, lower intelligence quotient (IQ) scores, impaired executive functioning, behavioral challenges, delays in expressive and receptive language development, and an increased risk of growth failure. In addition, the deficits of BPD have been found to influence much more than just physical health; BPD survivors have been noted to have higher rates of health care use, starting with the initial hospitalization and continuing with therapy and specialist follow-up, as well as impairments in quality of life, both physical and psychological, that continue into adulthood. The long-term consequences of BPD may best be addressed through future research, including better understanding of the pathophysiologic mechanisms leading to BPD, further comparisons between newborns with BPD and those without, and long-term assessment and management of BPD patients as adults.
INTRODUCTION: Acetaminophen (APAP) overdose is the most common cause of acute liver failure in the United States. We report a case of a patient who presented with acetaminophen overdose and was successfully treated with N-acetylcysteine (NAC) and 4-methylpyrazole (4-MP). CASE PRESENTATION:A 58-year-old female with history of alcohol abuse, hypertension, and hyperlipidemia presented with abdominal pain, nausea, and vomiting. Patient had fallen several days prior, resulting in rib fractures, and had been taking APAP for pain relief. Vital signs were within normal limits. Physical exam showed a lethargic, encephalopathic patient who only followed simple commands and had right upper quadrant abdominal tenderness. Labs revealed total bilirubin 6.4, AST 19816, ALT 5544, INR 3.7, acetaminophen level 58.3, lactic acid 12.2, creatinine 3.1, lipase 1187, and ammonia 82. Imaging was consistent with hepatic steatosis. Patient was treated with aggressive fluid resuscitation for pancreatitis; NAC and 4-MP for acetaminophen toxicity; lactulose and rifaximin for hepatic encephalopathy; vitamin K for coagulopathy; and albumin, octreotide, and midodrine for hepatorenal syndrome. Mental status and lab abnormalities gradually improved and acetaminophen level became undetectable.DISCUSSION: Our patient presented with unintentional APAP overdose. She likely had underlying chronic liver disease, as evidenced by hepatic steatosis on imaging, due to alcohol abuse. This likely made her more susceptible to liver injury, even with therapeutic doses of APAP.The pathogenesis APAP-induced hepatotoxicity starts with the conversion of APAP to N-acetyl-pbenzoquinone imine (NAPQI) by cytochrome P450 enzymes, which is detoxified by conjunction with glutathione.[1] When excessive amounts of APAP are ingested, hepatic glutathione levels are depleted, resulting in oxidant stress. NAC, the current standard of care and only clinically approved treatment for APAP overdose, attempts to limit this by accelerating glutathione synthesis and subsequent scavenging of NAPQI.[2]Recent literature has suggested that 4-MP may also be beneficial for attenuating liver injury in APAP overdose. 4-MP is classically known for its inhibition of alcohol dehydrogenase in methanol or ethylene glycol poisoning. However, it is unique in that it also directly inhibits CYP2E1, one of the major enzymes involved in the generation of NAPQI. 4-MP has been shown to be effective at preventing APAP-induced liver injury in mice and human hepatocytes and limiting oxidative metabolism in five human volunteers who ingested supratherapeutic APAP doses.[1,2] It may also protect against APAP-induced nephrotoxicity via a similar mechanism.[3] CONCLUSIONS: In patients presenting with APAP overdose, combination therapy with NAC and 4-MP may provide complementary protective effects through targeting of different therapeutic pathways.
Waterhouse-Friderichsen syndrome (WFS) is a rare, highly fatal disease that is the result of adrenal gland hemorrhage and infarction, typically due to Neisseria meningitidis infection. [1] We report a case of a patient who developed WFS secondary to Haemophilus influenzae type b (Hib) bacteremia. CASE PRESENTATION:A 19-year-old male with no medical history presented with vomiting and diarrhea for 2 days. Patient was febrile to 103.1 degrees Fahrenheit, hypotensive to 60/23, and tachycardic to 170/min. Labs showed WBC 7.9, platelets 98, creatinine 5.3, lactic acid 9.9, procalcitonin 256, and troponin peak 44.509. Respiratory viral panel and blood cultures were positive for rhinovirus and Hib, respectively. CT chest revealed scattered bilateral groundglass opacities. Patient had cardiac arrest x2. He was intubated and started on vasopressors/inotropes, antimicrobials, and renal replacement therapy. Echocardiogram showed ejection fraction (EF) 10-15%, necessitating intra-aortic balloon pump placement and veno-arterial extracorporeal membrane oxygenation (VA ECMO). Hospital course was complicated by the development of purpura fulminans, disseminated intravascular coagulation (DIC), rhabdomyolysis, heart block requiring transvenous pacemaker, and candida albicans fungemia. Patient was ultimately diagnosed with WFS and treated with hydrocortisone, resulting in hemodynamic improvement and weaning of circulatory support. Despite this, he eventually succumbed to his illness and the complications mentioned above. DISCUSSION: While Neisseria meningitidis accounts for the majority of cases of WFS, other bacteria, such as Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus, and Pseudomonas aeruginosa, have been implicated.[2] Suspicion should be raised in any patient presenting with fever, purpura, coagulopathy, and signs of adrenal insufficiency. [1] Diagnosis is confirmed by CT scan showing adrenal hemorrhage.[2] Mortality rates are as high as 50%, particularly when there are delays in diagnosis and subsequent treatment with corticosteroids.[1,2]Our patient presented with Hib bacteremia of unclear etiology. One possible explanation is pneumonia, as evidenced by groundglass opacities on CT chest, but these may be better explained by concurrent rhinovirus infection. He developed the bacteremia despite being up to date on immunizations and having vaccine titers, including Hib, within the protective range. Other immune deficiency workup was unrevealing. WFS was suspected but could not be confirmed with imaging due to hemodynamic instability and significant vasopressor support.CONCLUSIONS: WFS is an uncommon cause of adrenal insufficiency that requires prompt diagnosis and treatment. It should be considered in any patient presenting with septic shock, regardless of the causative organism.
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