Congestive Heart Failure
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
Pulmonary edema causes signs and symptoms that can mimic an exacerbation of COPD. The edema may be the primary symptom when the patient has no history of cardiac disorders. An immediate chest X-ray is usually sufficient for diagnosis and reveals extreme interstitial edema. If the diagnosis is still not confirmed, the serum brain natriuretic peptide (BNP)/N-terminal (NT)-prohormone BNP levels can be measured. They are elevated if pulmonary edema is present, but are normal if COPD is exacerbated. Other evaluations include blood tests, ECG, and pulse oximetry. The blood tests include cardiac biomarkers, BUN, electrolytes, and creatinine. For extremely ill patients, arterial blood gas measurements are taken. To determine the cause of pulmonary edema and select the best treatment, echocardiography may be done. Other factors to evaluate include severe hypoxemia and carbon dioxide retention, which is a late and severely negative sign of secondary hypoventilation.
Unusual Inherited Pulmonary Diseases Which Provide Clues to Pulmonary Physiology and Function
Stephen D. Litwin in Genetic Determinants of Pulmonary Disease, 2020
Acute mountain sickness is a relatively common affliction among persons rapidly ascending to high altitudes. It is well known to such pioneer scientists as Barcroft [132] and Monge [133]. The symptoms of headache, insomnia, loss of appetite, and breathlessness are usually mild and transient. In a small number of individuals, however, these symptoms are followed by the rapid development of pulmonary edema which is sometimes fatal. The disease is of considerable interest because (1) it has a tendency to occur in young, healthy individuals with no prior evidence of cardiopulmonary disease, (2) the causative factor, hypoxia, may be important in other forms of pulmonary edema, such as that induced by heroin, (3) it may provide a clue in the study of the mechanism of hypoxic pulmonary vasoconstriction, and (4) the pathogenesis of the disorder has not thus far been elucidated.
Chronic hypertension and acute hypertensive crisis
Hung N. Winn, Frank A. Chervenak, Roberto Romero in Clinical Maternal-Fetal Medicine Online, 2021
If a hypertensive crisis is suspected, then diagnosis, assessment, and therapy should proceed at equal pace. In the setting of hypertensive emergency, speed of intervention is important in limiting complications. A history should be obtained, focusing on any known history of hypertension, medications (prescribed, over-the-counter, and illicit), obstetric history, and symptoms. Blood pressure should be measured in each arm, with the patient sitting, using the correctly sized cuff. The remainder of the physical examination should incorporate assessment for pulmonary edema, peripheral pulses, and neurologic evaluation. In the nonpregnant patient with hypertensive crisis, fundoscopic examination of the retinas and auscultation of the flanks for bruits in the renal arteries are recommended as well (53), but in the hands of an obstetrician–gynecologist inexperienced in these examinations, they are likely to be of low yield.
Soft tissue calcifications secondary to Hymenoptera stings: a potential prognostic CT imaging sign in pediatric patients
Published in Clinical Toxicology, 2018
Wen-Jun Liu, Wei Li, Yang Tang, Si-Jie Gao, Fang Fang, Feng Xu, Ye Xu
Our HS patients were all treated with the followed regimen: (1) glucocorticoid (methylprednisolone administrated intravenously every 12 h at a dose of 8 mg/kg/day; the dose would be tapered when clinical symptoms and lab parameters relieved); (2) antihistamine (loratadine taken orally at a dose of 5mg/day for body weight ≤30 kg or 10 mg/day for body weight >30 kg); (3) sequential blood purification therapies included plasma exchange (PE), hemoperfusion (HP) or intermittent hemodiafiltration (HDF) simultaneously in the acute stage, and then intermittent hemodiafiltration (IHDF) or hemodialysis (IHD) in the remission stage would be performed when one of the following indications presented: (a) multiple organ failure (MOF); (b) total bilirubin (TBIL) > 20 μmol/L with elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST); (c) serum creatinine (SCR) 2.0–2.9 times higher than baseline or urine output < 0.5 mL/kg/h for ≥ 12 h; (d) apparent soy sauce-colored urine associated with blood urea nitrogen (BUN) > 28.6 mmol/L; (e) acute pulmonary edema; (f) severe metabolic acidosis (blood pH < 7.2); (g) severe hyperkalemia (serum potassium concentration > 6.5 mmol/L); (4) intubation and mechanical ventilation would be utilized if respiratory failure developed; (5) supportive symptomatic treatments, including cardioprotectants (creatine phosphate disodium salt and vitamin C), liver-protection drugs (atomolan, vitamin K1, ademetionine or ornithine aspartate), antibiotics, etc.
Scorpion envenomation: a deadly illness requiring an effective therapy
Published in Toxin Reviews, 2021
Faez Amokrane Nait Mohamed, Fatima Laraba-Djebari
Sweating is a clinical sign resulting from an uncontrollable catecholamine release and from sympathic and parasympathic nervous system activity (Sedziwy et al.1968). It is more marked in cases with pulmonary edema (Abroug et al.2020). Anxiety and agitation are important indicators of the severity of scorpion envenomation and can be associated with other neurological symptoms such as convulsions (Aboumaâd et al.2014, Yang et al.2014); it is well associated with an increase of sympathetic tone swelling left ventricular after-load and causing intense vasoconstriction, thus raising left ventricular filling pressures and inducing elevated pulmonary artery wedge pressures, leading to hydrostatic pulmonary edema and cardiac dysfunction (Bouaziz et al.2006, Bahloul et al.2013). Other neurological problems may appear, resulting from hypertensive encephalopathy (Rebahi et al.2015). Pulmonary edema is preceded by high blood pressure, which could lead to neurological damage, which could explain the observed neurological signs in these patients (Bahloul et al.2013).
Management of fluid status and cardiovascular function in patients with diffuse skin inflammation
Published in Journal of Dermatological Treatment, 2019
Arash Taheri, Amanda D. Mansouri, Parisa Mansoori, Rahimullah Imran Asad
Upon admission, the patient’s blood pressure was 90/50 and her heart rate was 100 (baseline values: blood pressure – 125/80; heart rate – 80). She did not have any jugular vein distension, and the results of the pulmonary exam were normal. She had severe peripheral pitting edema, mainly on the lower extremities. Her labs, including creatinine, were within a normal range. However, the patient reported dark yellow urine with reduced volume over the past few days. The primary team determined the patient was dehydrated and began intravascular infusion of normal saline. The patient received 2 l of normal saline in the first 24 h and was encouraged to eat and drink more. Twenty-four hours after starting the treatments, there was some improvement in the patient’s skin erythema; however, she was short of breath and hypoxic, with a high jugular venous pulse. Her blood pressure was 100/80 and heart rate was 100. A pulmonary exam and chest X-ray indicated pulmonary edema. The normal saline infusion was stopped, and 40 mg of furosemide was administered intravenously. The patient’s breathing improved in 5 h after significant diuresis. An echocardiogram revealed no evidence of heart disease. The intravascular volume overload and ensuing pulmonary edema were thought to be secondary to intravascular fluid administration and also to glucocorticoid use. The patient received one more dose of furosemide, continued on the same dose of prednisone, and was discharged on day three of admission after significant improvements in her erythema and edema.