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1
Bruno, Cosimo Marcello, and Maria Valenti. "Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review." Journal of Biomedicine and Biotechnology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/915150.
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The authors describe the pathophysiological mechanisms leading to development of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on outcome and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with emphasis on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are also examined, and practical considerations for a correct diagnosis are provided.
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Friis, Ulla G., Ronni Plovsing, Klaus Hansen, Bent G. Laursen, and Birgitta Wallstedt. "Teaching acid/base physiology in the laboratory." Advances in Physiology Education 34, no. 4 (December 2010): 233–38. http://dx.doi.org/10.1152/advan.90197.2008.
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Acid/base homeostasis is one of the most difficult subdisciplines of physiology for medical students to master. A different approach, where theory and practice are linked, might help students develop a deeper understanding of acid/base homeostasis. We therefore set out to develop a laboratory exercise in acid/base physiology that would provide students with unambiguous and reproducible data that clearly would illustrate the theory in practice. The laboratory exercise was developed to include both metabolic acidosis and respiratory alkalosis. Data were collected from 56 groups of medical students that had participated in this laboratory exercise. The acquired data showed very consistent and solid findings after the development of both metabolic acidosis and respiratory alkalosis. All results were consistent with the appropriate diagnosis of the acid/base disorder. Not one single group failed to obtain data that were compatible with the diagnosis; it was only the degree of acidosis/alkalosis and compensation that varied.
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Basok, Anna B., Yosef-S. Haviv, Boris Rogachev, and Marina Vorobiov. "Renal Tubular Acidosis Type I with Prominent Hypokalemia and Nephrolithiasis as a Presentation of Sjögren’s/Systemic Lupus Erythematosus Disease." Case Reports in Nephrology and Dialysis 11, no. 2 (August 12, 2021): 247–53. http://dx.doi.org/10.1159/000515050.
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Female patient, suffering from nephrolithiasis, at the age of 32 was admitted for renal colic caused by a stone obstructing UP junction with left hydronephrosis. Nephrostomy was placed, resulting in brisk diuresis. Severe metabolic acidosis with normal anion gap and urine pH of 6.5 was noted. Potassium level dropped to extremely low level (1.6 mEq/L), causing muscle paralysis and respiratory failure, necessitating mechanical ventilation. The patient was treated by potassium chloride infusion, followed by correction of severe metabolic acidosis by sodium bicarbonate. Diagnosis of distal type renal tubular acidosis type I (dRTA) was made based on normal anion gap metabolic acidosis, alkaline urine, hypokalemia, and nephrolithiasis. Five years later, the patient presented with severe hypoxia, lung opacities, and bronchiolitis obliterans organizing pneumonia which was confirmed by bronchoscopy with lung tissue biopsy. Concurrently, the patient presented with dry mouth, pruritus, skin rash with hypocomplementemia, elevated anti-DNA, anti-Ro, and anti-SmAb. Diagnosis of overlap Sjögren’s/systemic lupus erythematosus disease was done and treatment by hydroxychloroquine, prednisone, and azathioprine was started. Possible presence of Sjögren’s syndrome should be considered in adult patients with unexplained dRTA.
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McGonigle, Reid, and Robert A. Woods. "Take my breath away: a case of lactic acidosis in an asthma exacerbation." CJEM 13, no. 04 (July 2011): 284–88. http://dx.doi.org/10.2310/8000.2011.110236.
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ABSTRACT:A 36-year-old male with a history of chronic asthma presented to an emergency department with shortness of breath consistent with an asthma exacerbation. He had persistent tachypnea following inhaled bronchodilator treatment; thus, the workup and differential diagnosis were expanded. He was found to have a mixed respiratory alkalosis and metabolic acidosis with elevated serum lactate without an obvious cause and was admitted to hospital. His case was reviewed, and the lactic acidosis was thought to be caused by inhaled β2-agonist use. Emergency physicians should be aware of the potential side effects of inhaled β2-agonists as lactic acidosis may complicate clinical assessment and management of asthma exacerbations and lead to unnecessary and potentially dangerous escalations in therapy.
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Najout, Hamza, Mohamed Moutawakil, Abdelghafour Elkoundi, Nawfal Doghmi, and Hicham Bekkali. "Salbutamol-induced severe lactic acidosis in acute asthma." SAGE Open Medical Case Reports 8 (January 2020): 2050313X2096902. http://dx.doi.org/10.1177/2050313x20969027.
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Selective beta-adrenoceptor agonists are worldwide prescribed to manage bronchial obstruction. However, they expose to a potential risk of hyperlactatemia and lactic acidosis even with normal doses. The mechanism still poorly understood and suggested that salbutamol diverts the metabolism of pyruvate acid from Krebs cycle toward lactate formation. We report the case of a 42-year-old patient, admitted to intensive care unit for acute severe asthma. He presented a transient lactic acidosis over the first 48 h, following an excessive use of salbutamol. The metabolic acidosis caused tachypnea, as a compensatory mechanism, leading to respiratory failure. The diagnosis of salbutamol-induced lactic acidosis must be made by elimination and only accepted after deleting the other causes. The main clinical character is the worsening of dyspnea despite regression of bronchospasm. It is transient and usually normalizes within 24–48 h after stopping or decreasing doses of salbutamol.
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Latif, Azka, Aheli Arce Gastelum, Akshat Sood, and Joseph Thilumala Reddy. "Euglycaemic diabetic ketoacidosis in a 43-year-old woman with type 2 diabetes mellitus on SGLT-2 inhibitor (empagliflozin)." BMJ Case Reports 13, no. 6 (June 2020): e235117. http://dx.doi.org/10.1136/bcr-2020-235117.
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We report a case of euglycaemic diabetic ketoacidosis (EDKA) in a 43-year-old woman with type 2 diabetes mellitus who presented to the emergency department with problems of vomiting, cough, shortness of breath and generalised weakness after following a ketogenic diet for 2 weeks. Therapy with sodium glucose transport protein-2 empagliflozin had been started 2 months prior. Initial evaluation revealed high anion gap metabolic acidosis with blood glucose level of 169 mg/dL. Treatment for EDKA with fluid resuscitation, intravenous insulin and dextrose resolved her acidosis and symptoms in less than 24 hours. Empaglifozin was discontinued on discharge. This entity represents a diagnostic challenge since the differential diagnosis is broad with a potentially misleading clinical presentation that can result in delayed diagnosis and adverse outcomes including acute kidney injury, multiple electrolyte abnormalities, cerebral oedema, acute respiratory distress syndrome, shock and death.
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Moore, Darlene. "Medium-Chain Acyl-CoA Dehydrogenase Deficiency: A Case Presentation." Neonatal Network 24, no. 5 (September 2005): 7–13. http://dx.doi.org/10.1891/0730-0832.24.5.7.
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When an infant presents with hypoglycemia, acidosis, hepatomegaly, and respiratory arrest, the neonatal team must be alert to the possibility of a metabolic disorder. Among those to be considered is medium-chain acyl-CoA dehydrogenase deficiency, which occurs in 1 in 10,000–23,000 live births. Recognizing and treating this disorder early could decrease the morbidity and mortality associated with the diagnosis.
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Dernoncourt, A., J. Bouchereau, C. Acquaviva-Bourdain, C. Wicker, P. De Lonlay, C. Gourguechon, H. Sevestre, P. E. Merle, J. Maizel, and C. Brault. "Myogenic Disease and Metabolic Acidosis: Consider Multiple Acyl-Coenzyme A Dehydrogenase Deficiency." Case Reports in Critical Care 2019 (December 22, 2019): 1–7. http://dx.doi.org/10.1155/2019/1598213.
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Background. Multiple acyl-coA dehydrogenase deficiency (MADD) is a rare, inherited, autosomal-recessive disorder leading to the accumulation of acylcarnitine of all chain lengths. Acute decompensation with cardiac, respiratory or hepatic failure and metabolic abnormalities may be life-threatening. Case Presentation. A 29-year-old woman presented with severe lactic acidosis associated with intense myalgia and muscle weakness. The clinical examination revealed symmetric upper and lower limb motor impairment (rated at 2 or 3 out of 5 on the Medical Research Council scale) and clear amyotrophy. Laboratory tests had revealed severe rhabdomyolysis, with a serum creatine phosphokinase level of 8,700 IU/L and asymptomatic hypoglycemia in the absence of ketosis. Electromyography revealed myotonic bursts in all four limbs. The absence of myositis-specific autoantibodies ruled out a diagnosis of autoimmune myositis. Finally, Acylcarnitine profile and gas chromatography–mass spectrometry analysis of organic acids led to the diagnosis of MADD. A treatment based on the intravenous infusion of glucose solutes, administration of riboflavin, and supplementation with coenzyme Q10 and carnitine was effective. Lipid consumption was strictly prohibited in the early stages of treatment. The clinical and biochemical parameters rapidly improved and we noticed a complete disappearance of the motor deficit, without sequelae. Conclusion. A diagnosis of MADD must be considered whenever acute or chronic muscle involvement is associated with metabolic disorders. Acute heart, respiratory or hepatic failure and metabolic abnormalities caused by MADD may be life-threatening, and will require intensive care.
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Mendez, Yamely, Francisco E. Ochoa-Martinez, and Tatiana Ambrosii. "Chronic Obstructive Pulmonary Disease and Respiratory Acidosis in the Intensive Care Unit." Current Respiratory Medicine Reviews 15, no. 2 (December 10, 2019): 79–89. http://dx.doi.org/10.2174/1573398x15666181127141410.
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Chronic obstructive lung disease is a common and preventable disease. One of its pathophysiological consequences is the presence of carbon dioxide retention due to hypoventilation and ventilation/perfusion mismatch, which in consequence will cause a decrease in the acid/base status of the patient. Whenever a patient develops an acute exacerbation, acute respiratory hypercapnic failure will appear and the necessity of a hospital ward is a must. However, current guidelines exist to better identify these patients and make an accurate diagnosis by using clinical skills and laboratory data such as arterial blood gases. Once the patient is identified, rapid treatment will help to diminish the hospital length and the avoidance of intensive care unit. On the other hand, if there is the existence of comorbidities such as cardiac failure, gastroesophageal reflux disease, pulmonary embolism or depression, it is likely that the patient will be admitted to the intensive care unit with the requirement of intubation and mechanical ventilation.
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van Amesfoort, Jojanneke Epke, Dominique E. Werter, Rebecca C. Painter, and Frederik J. R. Hermans. "Severe metabolic ketoacidosis as a primary manifestation of SARS-CoV-2 infection in non-diabetic pregnancy." BMJ Case Reports 14, no. 4 (April 2021): e241745. http://dx.doi.org/10.1136/bcr-2021-241745.
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We present a case of a metabolic acidosis in a term-pregnant woman with SARS-CoV-2 infection.Our patient presented with dyspnoea, tachypnoea, thoracic pain and a 2-day history of vomiting, initially attributed to COVID-19 pneumonia. Differential diagnosis was expanded when arterial blood gas showed a high anion gap metabolic non-lactate acidosis without hypoxaemia. Most likely, the hypermetabolic state of pregnancy, in combination with maternal starvation and increased metabolic demand due to infection, had resulted in metabolic ketoacidosis. Despite supportive treatment and rapid induction of labour, maternal deterioration and fetal distress during labour necessitated an emergency caesarean section. The patient delivered a healthy neonate. Postpartum, after initial improvement in metabolic acidosis, viral and bacterial pneumonia with subsequent significant respiratory compromise were successfully managed with oxygen supplementation and corticosteroids. This case illustrates how the metabolic demands of pregnancy can result in an uncommon presentation of COVID-19.
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Inamdar, Nusrat R., Anupama V. Mauskar, Minal Wade, and Ankita Shah. "Neurocognitive outcome in young child with Isovaleric Acidemia." International Journal of Contemporary Pediatrics 6, no. 6 (October 21, 2019): 2716. http://dx.doi.org/10.18203/2349-3291.ijcp20194580.
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Isovaleric Acidemia (IVA) is inherited as an autosomal recessive trait, caused by the deficiency of the enzyme isovaleryl CoA dehydrogenase. It has the prevalence of 1 in 62,500 (in parts of Germany) to 1 in 250,000 live births (in the United States). Acute episodes of metabolic decompensations may occur, which may mimic sepsis, ketosis or shock. Early diagnosis & early initiation of treatment has been reported to correlate with a good neurocognitive outcome. This is case of child presenting in Paediatric emergency department with fever, vomiting, increased respiratory activity and lethargy. Child had GCS score of 8/15, acidotic breathing, hypotonia with hyporeflexia. Sepsis screen, metabolic work up and neuroimaging were all normal except for high anion Gap acidosis with ketosis. So further neurometabolic screening work up was done in view of persistent metabolic acidosis, developmental delay, and bad obstetric history in mother. It revealed increased excretion of isovalerylglycine 1(IVG 1), Isovalerylglycine 2 (IVG2) Lactate, 3-Hydroxypropionate (3HP) and 3-Hydroxybutyrate (3 HB).Serum lactate 358.54 (control 1.1-208.1) confirming the diagnosis of Isovaleric Acidemia. After recovery from the acute attack, the patient was advised low-protein diet (1.0-1.5 g/kg/24 hrs.) and carnitine (100 mg/kg/24 hrs. orally) supplements. On follow up child is asymptomatic & showing neurological improvement as he started achieving further developmental milestones during 6 months follow up.Early diagnosis and early treatment of IVA cases definitely results in favorable outcome and better prognosis. But chronic intermittent cases presenting late should not be neglected, proper medical management can reverse neuromotor consequences in them also.
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TAKASAKI, YUJI. "Water and electrolyte metabolic error: Advances in diagnosis and treatment. Abnormality of acid-base equilibrium. Respiratory acidosis and respiratory alkalosis." Nihon Naika Gakkai Zasshi 86, no. 10 (1997): 1884–90. http://dx.doi.org/10.2169/naika.86.1884.
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Cekerevac, Ivan, Vojislav Cupurdija, Ljiljana Novkovic, Zorica Lazic, Marina Petrovic, Olgica Gajovic, and Romana Susa. "Unusual Respiratory Manifestations of Ankylosing Spondylitis – A Case Report." Serbian Journal of Experimental and Clinical Research 17, no. 4 (December 1, 2016): 357–60. http://dx.doi.org/10.1515/sjecr-2016-0036.
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Abstract A male patient, 54 years old, was initially admitted to the hospital because of fatigue he felt during the last month and swelling of the lower legs. Upon hospital admittance, gas exchange analysis showed global respiratory failure: pO2=6.1 kPa, pCO2=10.9 kPa, pH=7.35, A-a gradient = 1.0. Due to the existence of hypercapnia and decompensated respiratory acidosis, the patient was connected to a device for non-invasive mechanical ventilation. Reduced chest mobility was noticed, and the respiratory index value was decreased. Radiographs of the chest and thoracic and lumbo-sacral spine showed marked changes on the spine attributable to ankylosing spondylitis (AS). Radiographs of the sacroiliac joints showed reduced sacroiliac joint intraarticular space with signs of subchondral sclerosis. The diagnosis of AS was set on the basis of New York Criteria (bilateral sacroiliitis, grade 3) and clinical criteria (back pain, lumbar spine limitation and chest expansion limitation). HLA typing (HLA B27 +) confirmed the diagnosis of AS. Pulmonary function test proved severe restrictive syndrome. Polysomnography verified the existence of severe obstructive sleep apnoea (AHI =73). This was a patient with newly diagnosed AS, with consequent severe restrictive syndrome and global respiratory failure with severe obstructive sleep apnoea. Thee patient was discharged from the hospital with a NIV (global respiratory failure) device for home use during the night.
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Mandell, Ivy. "Serum Anion Gap in Metabolic Acidosis." Neonatal Network 28, no. 4 (July 2009): 252–54. http://dx.doi.org/10.1891/0730-0832.28.4.252.
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METABOLIC ACIDOSIS, DEFINED AS A pathophysiologic state characterized by an arterial pH <7.35 in the absence of an elevated partial pressure of carbon dioxide in arterial blood (PaCO2), is a common finding in the critically ill neonate. It is the result of excess acid production, decreased renal excretion of acid, or increased loss of base.1,2In the neonatal period, metabolic acidosis is most often the result of shock or severe liver or kidney failure. In rare cases, however, it may be a discrete finding suggestive of an inborn error affecting acid production or renal acid excretion.3Left untreated, this acidosis can disturb many cell functions, potentially resulting in respiratory distress, pulmonary vasoconstriction, right ventricular dysfunction, tachycardia, myocardial depression, increased intracranial pressure, hyperkalemia, insulin resistance, decreased affinity of oxygen for hemoglobin, abdominal distention, or vomiting.4Although the most common treatment for acidosis is to “correct” it with bicarbonate (HCO3−), this therapy is not without its potential adverse effects. Therefore, correction of the underlying cause is considered to be the most important therapeutic measure in the management of metabolic acidosis.3,5Calculation of the anion gap is a useful and inexpensive tool with which to develop a differential diagnosis for metabolic acidosis in the neonate. This column examines the usefulness and limitations of calculating the serum anion gap.
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Makharia, Archita, Manoj Lakhotia, Mudita Gupta, and Pradeep Lalwani. "Hypokalaemic quadriparesis with respiratory failure due to latent Sjogren syndrome." BMJ Case Reports 14, no. 7 (July 2021): e243057. http://dx.doi.org/10.1136/bcr-2021-243057.
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Sjogren’s syndrome (SS) is an autoimmune disease with involvement of multiple organs, including both glandular and extraglandular organs. Usually involvement of glandular organs manifests before the extraglandular ones, but when the sequence is reversed, diagnosis may be missed. Hypokalaemic quadriparesis in SS is not uncommon. Respiratory failure in hypokalaemia is not usually seen, but in SS, it has been reported. We report a case of a 55-year-old woman who presented with sudden onset flaccid quadriparesis and respiratory muscle paralysis secondary to severe hypokalaemia. On detailed investigation, she was detected to have distal renal tubular acidosis secondary to clinically inapparent and asymptomatic SS.
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Udaltsov, M. A., K. V. Pshenisnov, Yu S. Аleksandrovich, and V. A. Kaziakhmedov. "Acute methadone poisoning in children: diagnosis and treatment." Messenger of ANESTHESIOLOGY AND RESUSCITATION 17, no. 5 (November 2, 2020): 31–39. http://dx.doi.org/10.21292/2078-5658-2020-17-5-31-39.
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Methadone poisoning is one of the most common causes of unfavorable outcomes in children.The objective is to identify specific parameters of the course and intensive care for methadone poisoning in children.Subjects and methods. 30 children were examined. The average age made 16 (15‒17) years. The duration of treatment in ICU was 3 (1.5‒4.0) days.Results. The most frequent clinical manifestations of methadone poisoning included coma (40%), acute respiratory failure (70%), low body temperature (57%), and myosis (100%). By the admission, the oxygenation index was 4.5 r.u. 37% of patients had pronounced lactate acidosis. On day 1, the volemic support made 143 (124‒165)% of the estimated fluid demand. 21 (70%) children needed artificial pulmonary ventilation. The negative correlation was established between treatment duration in ICU, Glasgow coma scale (R = -0.41; p < 0.05), Glasgow-Pittsburgh coma scale (R = -0.52; p < 0.05) and urea concentration in blood within the first 24 hours (R = 0.44; p < 0.05).Conclusion. The main criteria determining the severity of the state of patients with acute methadone poisoning include the level of depression of consciousness, the presence of acute respiratory and renal failure.
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Rafique, Muhammad. "Clinical Spectrum of Propionic Acidaemia." Journal of Nutrition and Metabolism 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/975964.
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Objectives. To evaluate the clinical features, physical findings, diagnosis, and laboratory parameters of the patients with propionic acidaemia (PA).Methods. The records of diagnosed cases of propionic acidaemia were reviewed, retrospectively.Results. Twenty-six patients with PA had 133 admissions. The majority (85%) of the patients exhibited clinical manifestations in the 1st week of life. Regarding clinical features, lethargy, fever, poor feeding, vomiting, dehydration, muscular hypotonia, respiratory symptoms, encephalopathy, disturbance of tone and reflexes, and malnutrition were observed in 51–92% admissions. Metabolic crises, respiratory diseases, hyperammonaemia, metabolic acidosis, hypoalbuminaemia, and hypocalcaemia were observed in 30–96% admissions. Pancytopenia, ketonuria, hypoproteinemia, hypoglycaemia, and mildly disturbed liver enzymes were found in 12–41% admissions. Generalised brain oedema was detected in 17% and cerebral atrophy in 25% admissions. Gender-wise odd ratio analysis showed value of 1.9 for lethargy, 1.99 for respiratory diseases, 0.55 for anaemia, and 1.82 for hypocalcaemia.Conclusion. Propionic acidaemia usually presents with wide spectrum of clinical features and disturbances of laboratory parameters in early neonatal age. It is associated with significant complications which deteriorate the patients’ quality of life. Perhaps with early diagnosis of the disease and in time intervention, these may be preventable.
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Anand, Neesha, Roberta M. Leu, Dawn Simon, and Ajay S. Kasi. "Recurrent apnoea and respiratory failure in an infant: congenital central hypoventilation syndrome with a novel PHOX2B gene variant." BMJ Case Reports 14, no. 3 (March 2021): e239633. http://dx.doi.org/10.1136/bcr-2020-239633.
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A 20-day-old term infant presented with recurrent apnoea, lethargy and respiratory failure. Examination revealed episodes of apnoea and desaturation to 85% without any signs of respiratory distress requiring initiation of non-invasive positive pressure ventilation (NPPV). Capillary blood gas was indicative of respiratory acidosis and serum bicarbonate was elevated at 35 mmol/L. Chest radiograph, echocardiogram and evaluations for infectious aetiologies resulted normal. Due to inability to wean off NPPV with ensuing apnoea and desaturation, polysomnogram was performed and showed central and obstructive sleep apnoea, hypoxaemia and hypoventilation. Central apnoeas and hypoventilation were worse in non-rapid eye movement sleep. Paired-like homeobox 2B genetic studies showed a novel non-polyalanine repeat mutation (c.429+1G>A) establishing the diagnosis of congenital central hypoventilation syndrome (CCHS). Our case highlights the utility of polysomnography in the evaluation of term infants with apnoea. Although rare, clinicians should consider a diagnosis of CCHS in the evaluation of infants with apnoea and hypoventilation.
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Dantas, Gabriela N., Bianca P. Santarosa, Fernando J. Benesi, Vitor Hugo Santos, and Roberto C. Gonçalves. "Clinical and blood gas analysis of calves conceived by artificial insemination, in vitro fertilization and animal cloning." Pesquisa Veterinária Brasileira 39, no. 7 (July 2019): 485–91. http://dx.doi.org/10.1590/1678-5150-pvb-5971.
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ABSTRACT: In order for successful extra-uterine adaptation to occur, it is necessary for the neonate to be able to establish its respiratory functions effectively, guaranteeing efficient oxygenation and good vitality. Respiratory disorders are the major cause of death during the neonatal period in cattle, and this mortality is even more significant when it comes to calves originated by in vitro fertilization (FIV) or animal cloning (CA). Blood gas analysis assesses acid-base balance changes effectively, and when associated with the neonate’s clinical examination, provides subsidies for accurate diagnosis and early treatment of neonatal maladaptation. The objective of this study was to study neonates born from artificial insemination (IA) and to compare them to calves conceived by FIV and CA, regarding blood gas and clinical examination. For that, 20 AI calves, 15 FIV calves, and 15 cloned calves were evaluated immediately after calving and at 6, 12, 24 and 48 hours of life. At all experimental times, venous blood samples were collected for blood gas and clinical examination was performed. In the postpartum evaluation, Apgar score and column length and respiratory amplitude measurements were used. IVF animals showed no alterations, resembling Group IA calves. The calves from CA showed more pronounced acidosis postpartum than expected physiological acidosis mixed for neonates, with decreasing values of bicarbonate (HCO3-), and base excess (BE) and the increase in carbon dioxide pressure (PCO2) when compared to the other groups. This disorder may have reflected lower mean values of Apgar scores and increased heart and respiratory rates. Intensive follow-up of these neonates is suggested, with monitoring by clinical and hemogasometric examination for early diagnosis of this condition and treatment based on oxygen therapy and bicarbonate replacement.
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Verheijen, Paul M., Lukas A. Lisowski, Phillip Stoutenbeek, J. François Hitchcock, Joel I. Brenner, Joshua A. Copel, Charles S. Kleinman, Erik J. Meijboom, and Ger B. W. E. Bennink. "Prenatal diagnosis of congenital heart disease affects preoperative acidosis in the newborn patient." Journal of Thoracic and Cardiovascular Surgery 121, no. 4 (April 2001): 798–803. http://dx.doi.org/10.1067/mtc.2001.112825.
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Sousa, Rejane dos Santos, Francisco Leonardo Costa de Oliveira, Mailson Rennan Borges Dias, Natalia Sato Minami, Leonardo do Amaral, Juliana Aparecida Alves dos Santos, Raimundo Alves Barrêto Júnior, Antonio Humberto Hamad Minervino, and Enrico Lippi Ortolani. "Characterization of Oligofructose-Induced Acute Rumen Lactic Acidosis and the Appearance of Laminitis in Zebu Cattle." Animals 10, no. 3 (March 4, 2020): 429. http://dx.doi.org/10.3390/ani10030429.
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The objective of this study was to characterize oligofructose-induced acute rumen lactic acidosis and its consequences in zebu cattle. We used 29 Nellore heifers which were submitted to experimental induction of laminitis by oligofructose excess. During the induction period, the animals underwent clinical examination, including laminitis diagnosis (hoof pressure testing and locomotion score) and blood and ruminal fluid sampling every six hours (over the initial 24 h) and every 12 h (up to 72 h), after the highest dose. Almost half of the animals (48.1%) required treatment with bicarbonate and saline to correct metabolic acidosis and dehydration. Due to this treatment, the animals were analyzed in treated (n = 13) and non-treated (n = 14) groups. The induction model promoted marked reduction in rumen pH, rumen anaerobiosis, carbon dioxide pressure, and increase in rumen lactate, blood osmolarity, and cortisol concentration. The animals treated had lower values of rumen pH and marked dehydration, evidenced by the increase in globular volume and serum urea. The clinical condition caused by excess oligofructose is severe, with the differential of the appearance of ephemeral fever and respiratory compensation against systemic acidosis, in addition to the frequent appearance of laminitis.
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Narita, Ikuyo, Michiko Shimada, Norio Nakamura, Reiichi Murakami, Takeshi Fujita, Wakako Fukuda, and Hirofumi Tomita. "Successful Resuscitation of a Patient with Life-Threatening Metabolic Acidosis by Hemodialysis: A Case of Ethylene Glycol Intoxication." Case Reports in Nephrology 2017 (2017): 1–4. http://dx.doi.org/10.1155/2017/9529028.
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Background. Ethylene glycol intoxication causes severe metabolic acidosis and acute kidney injury. Fomepizole has become available as its antidote. Nevertheless, a prompt diagnosis is not easy because patients are often unconscious. Here we present a case of ethylene glycol intoxication who successfully recovered with prompt hemodialysis. Case Presentation. A 52-year-old Japanese male was admitted to a local hospital due to suspected food poisoning. The patient presented with nausea and vomiting, but his condition rapidly deteriorated, with worsening conscious level, respiratory distress requiring mechanical ventilation, hypotension, and severe acute kidney injury. He was transferred to the university hospital; hemodialysis was initiated because of hyperkalemia and severe metabolic acidosis. On recovering consciousness, he admitted having ingested antifreeze solution. Thirty-seven days after admission, the patient was discharged without requiring HD. Conclusions. We reported a case of ethylene glycol intoxication who presented with a life-threatening metabolic acidosis. In a state of severe circulatory shock requiring catecholamines, hemodialysis should be avoided, and continuous hemodiafiltration may be a preferred approach. However, one should be aware of the possibility of intoxication by unknown causes, and hemodialysis could be life-saving with its superior ability to remove toxic materials in such cases.
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Mirzaee, Vahid, Zahra Riahi, Zahra Sharifzadeh, Moein Kardoust Parizi, and Amir Adinehpour. "Survey On Methanol Poisoning Epidemic in Rafsanjan City in Year 2013." Internal Medicine and Medical Investigation Journal 2, no. 3 (September 11, 2017): 84. http://dx.doi.org/10.24200/imminv.v2i3.47.
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Background: Examination and early detection of the methanol toxicity epidemic are very important, so identification and initiation of appropriate therapy can significantly reduce morbidity and mortality. Therefore, this study was aimed to investigation methanol poisoning epidemic in Rafsanjan city.Methods: This case series study was conducted in 252 patients with methanol poisoning in 2013 in the Ali-ibn-Abi-Talib hospital of Rafsanjan. Data were through interviews and records that were collected at hospital admission. Due to the large number of patients and the possible lack of ability of rapid measurement of serum levels of methanol and need of rapid intervention, treatment to reduce any further complications, early diagnosis and treatment were carried out by clinical history and interpretation of arterial blood gas test results. Data record on provided checklists and then analyzed using SPSS version 19.Results: The mean pH was 0.13±7.27. The most frequent clinical features were visual disturbances (39.7%), dyspnea (1.2%), and gastrointestinal symptoms (7.1%). There was a trend towards decreasing PCO2 with decreasing pH amongst the patients surviving. The opposite trend was demonstrated in the dying; the difference was highly significant by linear regression analyses (P< 0.001).Conclusions: Methanol poisoning still has a high morbidity and mortality, mainly because of late diagnosis and treatment. Respiratory arrest, coma and severe metabolic acidosis upon admission were strong predictors of poor outcome. Early admission and ability of respiratory compensation of metabolic acidosis were associated with survival.
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Perepelitsa, S. A., and E. F. Smerdova. "Differential Diagnosis of Congenital Pneumonia in Newborns with Low and Extremely Low Body Weight (Morphological Study)." General Reanimatology 14, no. 4 (September 2, 2018): 4–14. http://dx.doi.org/10.15360/1813-9779-2018-4-4-14.
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The purpose of the study is a comprehensive assessment of morphological changes in the placenta and lungs to detect early signs of congenital pneumonia in extremely premature infants.Materials and methods. Protocols of post-mortem examinations of 23 preterm newborns died from severe respiratory failure were analyzed. The average gestational age of the newborns was 26.4±2.7 weeks and the body weight at birth was 972.4±355.8 grams. In the sample, 78.3% of infants had an extremely low birth weight (ELBW). At birth, all newborns presented severe asphyxia. Newborn underwent several types of respiratory therapy since birth: Mechanical ventilation was performed in 65.2% of newborns since their birth, non-invasive ventilation was performed in 26.1% of cases, and 8.7% of patients underwent oxygenotherapy through a facial mask. In all cases, there was an unfavorable course of the neonatal period, a progressive deterioration of newborns' condition, and a lethal outcome. A comprehensive histological examination of the placenta and the lungs of deceased premature newborn infants was performed.Results. Congenital infections of different localizations remain the leading cause of death.Congenital pneumonia and generalized infections are clinically manifested at birth by severe perinatal hypoxia and respiratory failure. In the case of congenital pneumonia, the morphological patterns are polymorphic and characterize the severity of lung damage. For some newborns, these patterns include accumulation of exudates and fibrin, segmented leukocytes, fragments of basophilic coccal microflora, and a large number of colony forming bacilli, and desquamated alveolocytes with a deformed nucleus are visualized in the deformed lumen of the alveoli and bronchi. Diffuse lymphoid-leukocyte infiltration in the septa and respiratory parts of the lungs are typical for other infants. Histological examination find lumpy or lamellar eosinophilic hyaline membranes in alveoli in specimens from these newborns. Diffuse, focal or confluent segmentonuclear infiltration in various lung structures is commonly combined with hyaline membranes of various localizations and sizes. Hyaline membranes were detected in 93.5% of cases.Conclusion. Very early preterm delivery is associated with intrauterine pneumonia and systemic infection in extremely premature infants. Early clinical and laboratory signs of intrauterine infectious lung include severe perinatal hypoxia, very low Apgar score and laboratory test findings (hypoxaemia and decompensated metabolic lactate acidosis) that are resistant to standard resuscitation measures. Hypoxemia and decompensated metabolic acidosis persisting during the first hours of postnatal life indicate the severity of intrauterine lung damage and require a rapid change of treatment aimed at normalization of lung function, prevention of complications in the respiratory system, hemostasis and central nervous system. Clinicians should be better informed about the features of early postnatal adaptation of extremely premature infants with congenital pneumonia to provide appropriate treatment.
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Jecker, Nancy S. "Caring for “Socially Undesirable” Patients." Cambridge Quarterly of Healthcare Ethics 5, no. 4 (1996): 500–510. http://dx.doi.org/10.1017/s0963180100007398.
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Mr. Bernard was a homeless man, aged 58. His medical history revealed alcohol abuse, seizure disorder, and two suicide attempts. Brought to the emergency room at a local hospital after being found “semi-comatose,” his respiratory distress led to his being intubated and placed on a ventilator. The healthcare team suspected the patient ingested antifreeze. Transferred from that hospital to the intensive care unit (ICU) of the university hospital, his diagnosis was “high osmolar gap with high-anion gap metabolic acidosis, most likely secondary to ethylene glycol ingestion and renal insufficiency.”
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Kaye, William, Arnold Sladen, and Ronald Stewart. "The Mega Code for Advanced Cardiac Life Support (ACLS): Training and Performance Evaluation." Journal of the World Association for Emergency and Disaster Medicine 3, no. 1 (1987): 77–79. http://dx.doi.org/10.1017/s1049023x00028806.
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ACLS for cardiac arrest consists of basic life support, which includes mouth-to-mouth breathing and external chest compression; management of the airway with adjunctive equipment including intubation and ventilator support with supplemental oxygen; recognition of specific cardiac dysrhythmias and appropriate emergency therapy; electrical defibrillation and cardioversion; techniques for placement of intravenous lines; diagnosis of and therapy for acidbase abnormalities with particular emphasis on respiratory and metabolic acidosis; drug therapy during the pre-arrest phase, the cardiac arrest itself, and the period following resuscitation; and stabilization, to prevent cardio-respiratory arrest, and during the post-resuscitation period. In 1975, the American Heart Association developed an ACLS Training Program in which cognitive knowledge is presented at lectures and practical skills are taught and tested at several performance stations.
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Abdelmasih, Randa, Ramy Abdelmaseih, Faysal Rifai, Elio Paul Monsour, and Justin Reed. "SGLT2 Inhibitor Induced Euglycemic DKA (EDKA) With Proximal Renal Tubular Acidosis (RTA) as a Rare Fatal Complication in a Non-Insulin Dependent Diabetic Patient: A Challenging Dilemma." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A400—A401. http://dx.doi.org/10.1210/jendso/bvab048.815.
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Abstract Introduction: Diabetic Ketoacidosis (DKA) is characterized by a triad of hyperglycemia, acidemia, and ketonemia. Rarely, it would present with normal glucose levels making its diagnosis very challenging. The incidence of euglycemic DKA (eDKA) has increased with the introduction of the novel sodium-glucose cotransporter-2 inhibitors (SGLT2i). Currently, the reported incidence of SGLT2i induced DKA is 0.16–0.76 events per 1000 patient-years. We present a rare case of SGLT2i induced eDKA with proximal renal tubular acidosis (RTA). Case Presentation A 69 year-old male with type 2 diabetes mellitus presented to the hospital with severe respiratory distress, nausea and vomiting for 2 days. His home medications include metformin and canagliflozin. He was afebrile with respiratory rate 60 breaths/min. Arterial blood gas: pH 7.21, pCO2 9.2, pO2 223, HCO3 6. Blood glucose level was 120 mg/dl. Urinalysis was positive for large ketonuria >160 mg/dl and glycosuria >500 mg/dl. Serum anion gap and urine anion gap were elevated 29 mEq/L and 105 mEq/L respectively. Serum osmolarity and urine osmolality were elevated 296 mosm/kg and 653 mosm/kg respectively. Lactic acid was 5.3. Acetone was detected in blood. No source of infection was identified. Hemoglobin A1C was 5% and c-peptide was within normal range. Insulin and Islet cells antibodies were negative. DKA protocol was initiated until the anion gap closed. However, non-anion gap metabolic acidosis was persistent with profound hypophosphatemia. Repeat urinalysis showed glycosuria with pH ≤ 5.5, phosphaturia and generalized aminoaciduria. Ultimately, the patient elected to receive hospice care. Discussion: SGLT2i are currently recommended as second-line medications for type 2 diabetes mellitus. Their unique mechanism of action prevents glucose reabsorption from the proximal renal tubules. SGLT2i use is growing significantly, especially after recent clinical trials that demonstrated favorable protective effects. EDKA is precipitated by sepsis, acute illness, dehydration, or starvation. Once the diagnosis is suspected, SGLT2i should be stopped immediately. SGLT2i induced eDKA should be treated in a similar fashion as DKA. It is worth to note that SGLT2i half-life ranges from 11–17 hours, and despite drug discontinuation, glycosuria may persist for several days. What made our case unique and made the diagnosis challenging, was the normal blood glucose level, as well as other differentials that could have easily explained the acidosis including starvation ketosis and lactic acidosis. Also, the state of proximal RTA resembling renal Fanconi syndrome that occurred in correlation with canagliflozin therapy. To the best of our knowledge, this is the fourth reported case of proximal RTA with the use of canagliflozin resulting in life-threatening complications. The diagnosis was very challenging due to lack of awareness of this severe adverse effect.
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Glover Williams, Alessandra, Janet McNally, Julian Gaskin, and Ela Chakkarapani. "Preterm Infant with Congenital Tracheal Diverticulum in the Presence of Esophageal Atresia and Tracheoesophageal Fistula." Journal of Neonatal Surgery 7, no. 4 (October 6, 2018): 44. http://dx.doi.org/10.21699/jns.v7i4.741.
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A 32+4-week-preterm neonate was operated on day 1 for esophageal atresia with tracheoesophageal fistula with a tight primary anastomosis and closure of a tracheoesophageal fistula. Postoperatively, he needed ventilation for 6 days. Post-extubation, he needed continuous positive airway pressure support for increased work of breathing, increasing oxygen requirement, and respiratory acidosis when respiratory support was weaned. Further, during the post-operative period, he had right hemidiaphragmatic paresis and acute lifethreatening events requiring manual high-pressure, non-invasive positive pressure ventilation resuscitation. These complications were considered, and a computed tomography assisted by three-dimensional reconstruction was performed. This revealed a congenital tracheal diverticulum and severe tracheomalacia which was confirmed with microlaryngoscopy and bronchoscopy. The presentation and the diagnostic dilemma surrounding this rare diagnosis are discussed in this case report.
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Erdol, Sahin, and Halil Saglam. "Outcomes of mitochondrial derived diseases: a single-center experience." Journal of Pediatric Endocrinology and Metabolism 31, no. 4 (March 28, 2018): 399–405. http://dx.doi.org/10.1515/jpem-2017-0405.
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AbstractBackground:The purpose of this study is to help elucidate which part of the mitochondria is causing a problem through anamnesis, physical examination, and routine biochemical tests in the event of a suspected mitochondrial disease case.Methods:The data were obtained retrospectively from the medical records of 75 cases; the mitochondrial-derived disease (MDD) cases were observed in our center from 2011 to 2017.Results:The most commonly observed MDDs were oxidative phosphorylation disorders at 44%, followed by fatty acid oxidation disorder at 40%, pyruvate metabolism disorder at 12%, and ketone metabolism disorder at 4%, respectively. The most common clinical presentation at the time of referral to the hospital was metabolic acidosis (20%), and the most common symptom was respiratory distress (24%). There were abnormal findings in 84.3% of the cases subjected to cranial magnetic resonance imaging (MRI), with the most common being hyperintensity in the bilateral basal ganglia (49.0%).Conclusions:Anamnesis, physical examination, and simple laboratory data could provide some important clues in assessing MDD. Blood gas should definitely be measured in cases with respiratory symptoms, particularly if they have a history of consanguineous marriage or a sibling suffering from a similar disease. If metabolic acidosis exists in the blood gas, MDDs should absolutely be included in the differential diagnosis. Furthermore, ophthalmic and cardiac assessment and cranial MRI will also reveal significant data for diagnosing MDDs.
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Trovatelli, M., G. Sala, S. Romussi, and A. Boccardo. "An oesophageal benign stricture: Endoscopy treatment limitation and surgical management in a heifer." Veterinární Medicína 66, No. 6 (May 31, 2021): 272–77. http://dx.doi.org/10.17221/93/2020-vetmed.
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A 4-month-old female red Holstein Friesian heifer was referred with intermittent meteorism and regurgitation associated with poor weight gain. The subject showed a fair physical condition with an increased respiratory rate, normal food prehension, mastication, and swallowing activity. The blood gas analysis showed mild respiratory acidosis. An oral gastric tube introduction followed by an endoscopy confirmed the provisional diagnosis of benign oesophageal stenosis. An endoscopic balloon and bouginage did not result in any stricture release, probably due to the degree of fibrosis of the stenotic ring. A surgical approach with a mucosectomy was performed, which restored the normal oesophageal function. Based on the authors’ knowledge, this is the first description of a bovine oesophageal mucosectomy as a definitive surgical treatment for a stricture after the failure of both balloon dilation and a bougienage technique.
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Greenberger, Paul A. "Potentially (near) fatal asthma." Allergy and Asthma Proceedings 40, no. 6 (November 1, 2019): 403–5. http://dx.doi.org/10.2500/aap.2019.40.4257.
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Potentially (near) fatal asthma (PFA) defines a subset of patients with asthma who are at increased risk for death from their disease. The diagnosis of PFA should motivate treating physicians, health professionals, and patients to be more aggressive in the monitoring, treatment, and control of this high-risk type of asthma. A diagnosis of PFA is made when any one of the following are present: (1) a history of endotracheal intubation from asthma, (2) acute respiratory acidosis (pH < 7.35) or respiratory failure from acute severe asthma, (3) two or more episodes of acute pneumothorax or pneumomediastinum from asthma, (4) two or more episodes of acute severe asthma, despite the use of long-term oral corticosteroids and other antiasthma medications. There are two predominant phenotypes of near-fatal exacerbations: “subacute” exacerbation and “hyperacute” exacerbation. The best way to “treat” acute severe asthma is 3‐7 days before it occurs (i.e., at the onset of symptoms or change in respiratory function) and to optimize control of asthma by decreasing the number of symptomatic days and the days and/or nights that require rescue therapy and increasing baseline respiratory status in “poor perceivers.” PFA is treated with a multifaceted approach; physicians and health-care professionals should appreciate limitations of pharmacotherapy, including combination inhaled corticosteroid‐long-acting β-agonist products as well as addressing nonadherence, psychiatric, and socioeconomic issues that complicate care.
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Amendum, Paige, Shaukat Khan, Seiji Yamaguchi, Hironori Kobayashi, Yasuhiko Ago, Yasuyuki Suzuki, Betul Celik, et al. "Glycosaminoglycans as Biomarkers for Mucopolysaccharidoses and Other Disorders." Diagnostics 11, no. 9 (August 28, 2021): 1563. http://dx.doi.org/10.3390/diagnostics11091563.
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Glycosaminoglycans (GAGs) are present in proteoglycans, which play critical physiological roles in various tissues. They are known to be elevated in mucopolysaccharidoses (MPS), a group of rare inherited metabolic diseases in which the lysosomal enzyme required to break down one or more GAG is deficient. In a previous study, we found elevation of GAGs in a subset of patients without MPS. In the current study, we aim to investigate serum GAG levels in patients with conditions beyond MPS. In our investigated samples, the largest group of patients had a clinical diagnosis of viral or non-viral encephalopathy. Clinical diagnoses and conditions also included epilepsy, fatty acid metabolism disorders, respiratory and renal disorders, liver disorders, hypoglycemia, developmental disorders, hyperCKemia, myopathy, acidosis, and vomiting disorders. While there was no conclusive evidence across all ages for any disease, serum GAG levels were elevated in patients with encephalopathy and some patients with other conditions. These preliminary findings suggest that serum GAGs are potential biomarkers in MPS and other disorders. In conclusion, we propose that GAGs elevated in blood can be used as biomarkers in the diagnosis and prognosis of various diseases in childhood; however, further designed experiments with larger sample sizes are required.
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REDONDO-GONZÁLEZ, O., and J. M. TENÍAS-BURILLO. "A multifactorial regression analysis of the features of community-acquired rotavirus requiring hospitalization in Spain as represented in the Minimum Basic Data Set." Epidemiology and Infection 144, no. 12 (May 6, 2016): 2509–16. http://dx.doi.org/10.1017/s0950268816000881.
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SUMMARYOver 10% of acute rotavirus gastroenteritis (ARGE) requires hospitalization because of complications. The aggravating factors have been widely analysed, but in an isolated way. We aimed to explore the interrelationship between the clinical and epidemiological factors that characterize rotavirus hospitalizations in Spain using information from the Minimum Basic Data Set (MBDS). Using ICD-9-CM codes, we classified acute gastroenteritis (AGE) cases by principal diagnosis fields and then categorized their comorbidities, complications, and epidemiological features by secondary fields. A multivariable, logistic, step-wise regression model was then constructed. We identified 1657 ARGE cases from 17 415 cases of AGE. Rotavirus hospitalizations were associated with place of residence, age, and season (P < 0·0001), as well as with dehydration [odds ratio (OR) 12·44, 95% confidence interval (CI) 1·52–40·38], intravenous rehydration (OR 1·74, 95% CI 1·29–2·35), metabolic acidosis (OR 1·51, 95% CI 1·24–1·83), respiratory tract infections (RTIs) (OR 1·60, 95% CI 1·09–1·98), and concomitant AGE (OR 1·52, 95% CI 1·03–2·25). Dehydration was four times more likely in patients aged <5 years (OR 4·36, 95% CI 1·20–12·96) and was associated with acidosis when ARGE and RTI were present simultaneously (P < 0·0001). Specific co-infecting viruses may play a role in acute respiratory symptoms and aggravation of gastrointestinal manifestations of rotaviruses, thus leading to complications requiring hospitalization.
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Adrogué, Horacio J. "Diagnosis and Management of Severe Respiratory Acidosis: A 65-Year-Old Man With a Double-Lung Transplant and Shortness of Breath." American Journal of Kidney Diseases 56, no. 5 (November 2010): 994–1000. http://dx.doi.org/10.1053/j.ajkd.2010.04.024.
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Horikoshi, Rihito, Tadashi Kitamura, and Kagami Miyaji. "Ketoacidosis related to sodium glucose cotransporter 2 inhibitors after emergency coronary surgery." Interactive CardioVascular and Thoracic Surgery 29, no. 2 (April 9, 2019): 323–24. http://dx.doi.org/10.1093/icvts/ivz091.
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Abstract Sodium glucose cotransporter 2 inhibitors are currently widely used antihyperglycaemic medications that are considered to be associated with euglycaemic diabetic ketoacidosis. We report 2 cases of patients who received sodium glucose cotransporter 2 inhibitors until emergency coronary artery bypass grafting (CABG) and developed euglycaemic ketoacidosis after surgery; they were treated with sugar replenishment and insulin infusion. In one case, coronary angiography revealed a spastic change of the bypass graft possibly due to severe acidosis. A rapid diagnosis and proper intervention are crucial to achieve better outcomes with CABG.
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Ciceri, E., I. Moroni, G. Uziel, and M. Savoiardo. "Le encefalomiopatie mitocondriali." Rivista di Neuroradiologia 9, no. 6 (December 1996): 775–80. http://dx.doi.org/10.1177/197140099600900623.
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The mitochondrial encephalomyopathies are relatively rare neuromuscular diseases clinically characterised by myopathy and encephalopathy caused by structurally or functionally impaired mitochondria. The biochemical hallmark of this group of disorders is impaired mitochondrial energy production: Kreb's cycle, respiratory chain, oxidative phosphorylation and beta-oxidation of fatty acids. The presence of lactic acidosis and ragged red fibres, i.e. subsarcolemmal accumulations of abnormally sized mitochondria are highly indicative findings for mitochondrial disease. Classification and diagnostic criteria are based on biochemical findings with a search for specific enzyme deficit and molecular genetic information. Molecular genetic studies aim to identify the mitochondrial DNA changes responsible for the enzyme defect. Ragged red fibres are not essential for diagnosis as they are not present in some diseases. In rare cases, mitochondrial diseases are caused by nuclear DNA defects or, more commonly a mitochondrial DNA deficit. Diagnosis may prove difficult given the pathogenetic complexity and clinical and phenotypical variability of these conditions. Despite indirect symptoms of mitochondrial disease, the enzyme defect and genetic alteration cannot be identified in some cases. The mitochondrial encephalopathies can be classified according to the metabolic pathways involved into impaired transport ot uptake of energy, impaired Kreb's cycle or respiratory chain complexes or complex defects due to mitochondrial DNA changes.
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Rivera Nazario, Ivan Augusto, Arnaldo Nieves Ortiz, Jose Ayala Rivera, Kyomara Hernandez Moya, Arnaldo Rojas, Zahira Marie Lugo Lopez, Marina Torres Torres, et al. "An Atypical Presentation of Hyperosmolar Hyperglycemic State Induced by SARS CoV 2." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A366—A367. http://dx.doi.org/10.1210/jendso/bvab048.746.
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Abstract Hyperglycemic emergencies such as Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycemic State (HHS) are commonly precipitated by infectious processes. Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) is a novel infectious process prompting hyperglycemic crisis. SARS-CoV-2 at the level of the lungs affects ACE2 functioning which in turns decrease the B cells proliferation at the pancreas and hinders insulin secretion. Advanced age and comorbidities such as hypertension, cardiovascular disease and diabetes mellitus are considered to be a risk factors for severe illness and mortality between patients with SARS-CoV-2. We present the case of a 39-year-old woman with medical history of uterine fibroma, who presented with complains of general malaise, polyuria and polydipsia of one week evolution, associated with sore throat, subjective fever, dry cough, abdominal pain, nausea and vomiting. Physical examination remarkable for dry oral mucosa, decreased skin turgor, and prolonged capillary refills. Vital signs significant for hypertension, tachycardia, and tachypnea. Laboratory work up remarkable for glucose of 1321 mg/dL, HCO3- of 16 mEq/L, serum osmolality of 333 mOsm/kg, serum ketones positive and HbA1C of 15%. ABG’s showed pH of 7.33, PCO2 of 29.8 and a PAO2 of 158.5 mmHg for a high anion gap metabolic acidosis (AG of 15.3 mEq/L), non-anion gap metabolic acidosis with respiratory alkalosis. Chest X-ray revealed bilateral perihilar, peribronchial cuffing. SARS-CoV-2 PCR testing was positive. Clinical and laboratory workup met criteria for diagnosis of HHS and Diabetes Mellitus de Novo most likely secondary to SARS-CoV-2 infection. Patient was treated with aggressive IV hydration and insulin infusion with resolution of hyperglycemia, ketonemia and symptoms. SARS-CoV-2 infection can precipitate acute metabolic complications in patients with diabetes or unknown diagnosis of diabetes. The effect of the virus could be direct effect on β-cell function. To our knowledge, there are only a few cases reported of HHS precipitated by SARS-CoV-2 infection therefore medical awareness is important for early diagnosis of possible triggering factors such as COVID-19 and early management of patients presenting with new onset hyperglycemic emergencies.
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Wijburg, F. A., R. J. A. Wanders, E. M. van Lie Peters, G. D. Vos, H. G. Loggers, P. A. Bolhuis, N. H. Herzberg, et al. "NADH:Q1 oxidoreductase deficiency without lactic acidosis in a patient with leigh syndrome: Implications for the diagnosis of inborn errors of the respiratory chain." Journal of Inherited Metabolic Disease 14, no. 3 (May 1991): 297–300. http://dx.doi.org/10.1007/bf01811686.
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Hamzagic, Nedim, Tomislav Nikolic, Biljana Popovska Jovicic, Petar Canovic, Sasa Jacovic, and Dejan Petrovic. "Acute Kidney Damage: Definition, Classification and Optimal Time of Hemodialysis." Serbian Journal of Experimental and Clinical Research 20, no. 3 (September 1, 2019): 267–75. http://dx.doi.org/10.1515/sjecr-2017-0050.
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Abstract Acute damage to the kidney is a serious complication in patients in intensive care units. The causes of acute kidney damage in these patients may be prerenal, renal and postrenal. Sepsis is the most common cause of the development of acute kidney damage in intensive care units. For the definition and classification of acute kidney damage in clinical practice, the RIFLE, AKIN and KDIGO classifications are used. There is a complex link between acute kidney damage and other organs. Acute kidney damage is induced by complex pathophysiological mechanisms that cause acute damage and functional disorders of the heart (acute heart failure, acute coronary syndrome and cardiac arrhythmias), brain (whole body cramps, ischaemic stroke and coma), lung (acute damage to the lung and acute respiratory distress syndrome) and liver (hypoxic hepatitis and acute hepatic insufficiency). New biomarkers, colour Doppler ultrasound diagnosis and kidney biopsy have significant roles in the diagnosis of acute kidney damage. Prevention of the development of acute kidney damage in intensive care units includes maintaining an adequate haemodynamic status in patients and avoiding nephrotoxic drugs and agents (radiocontrast agents). The complications of acute kidney damage (hyperkalaemia, metabolic acidosis, hypervolaemia and azotaemia) are treated with medications, intravenous solutions, and therapies for renal function replacement. Absolute indications for acute haemodialysis include resistant hyperkalaemia, severe metabolic acidosis, resistant hypervolaemia and complications of high azotaemia. In the absence of an absolute indication, dialysis is indicated for patients in intensive care units at stage 3 of the AKIN/KDIGO classification and in some patients with stage 2. Intermittent haemodialysis is applied for haemodynamically stable patients with severe hyperkalaemia and hypervolaemia. In patients who are haemodynamically unstable and have liver insufficiency or brain damage, continuous modalities of treatment for renal replacement are indicated.
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Lonati, Davide, Carlo Alessandro Locatelli, Lucia Fenicia, Fabrizio Anniballi, Paolo Landri, Andrea Giampreti, Valeria Margherita Petrolini, Sarah Vecchio, and Luigi Manzo. "Fatal course of foodborne botulism in an eigth-month old Infant." Pediatric Reports 3, no. 4 (December 2, 2011): 31. http://dx.doi.org/10.4081/pr.2011.e31.
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An 8-month old girl, weighing 9 kg, was brought by her parents at 8.15 am to the Emergency Department (ED) for a progressive worsening of weakness and acute respiratory failure. On admission, the baby presented with poor oral intake, a weak cry and extremely weak muscular body control. Poor gag and suck, unreactive mydriasis, hypotonia, lethargy and absence of peristalsis were noted. Laboratory data showed severe respiratory acidosis. Chest X-ray, electroencephalography, encephalic CT scan and MRI were all normal, as were cerebrospinal fluid analysis and viral tests. Orotracheal intubation and continuous mechanical ventilation were applied. The patient received fluids, corticosteroids, aerosol therapy, large-spectrum antibiotics and enteral- nutrition. Further investigation revealed ingestion of an improperly prepared homecanned homogenized turkey meal. Type A botulinum neurotoxin was identified. Trivalent botulinum antitoxin, prostigmine and oral activated charcoal were administered. Generalized flaccid paralysis, areflexic bilateral mydriasis, gastric stasis and deep coma persisted for the duration of the hospital stay, and the patient died of severe respiratory failure and cardiac arrest 12 days after ED admission. Botulism poisoning should be suspected in any infant presenting with feeding difficulties, constipation, descendent paralysis or acute respiratory failure. Supportive treatment and antidotal therapy should be performed as soon as a clinical diagnosis is made. We describe a case of foodborne botulism in an 8-month old infant caused by ingestion of an improperly prepared home-canned homogenized turkey meal, representing the youngest fatal case reported in medical literature.
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Rüegg, Stephan. "Nonconvulsive Status Epilepticus in Adults: Types, Pathophysiology, Epidemiology, Etiology, and Diagnosis." Neurology International Open 01, no. 03 (June 2017): E189—E203. http://dx.doi.org/10.1055/s-0043-103383.
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AbstractNonconvulsive status epilepticus (NCSE) is defined by permanent electroclinical nonconvulsive epileptic activity or a series of nonconvulsive seizures without recovery to baseline. This “silent” manifestation of lasting neurological symptoms, like aphasia, confusion, etc., impedes easily recognizing NCSE. The most important diagnostic step often is to consider the possibility of NCSE. NCSE can only be confirmed by an immediate EEG recording. Epidemiological studies show slight preponderance of convulsive status epilepticus (CSE) over NCSE (60:40%); however, this might result from lack of recognition of NCSE because of its very unspectacular manifestation. Regarding pathophysiology, the neuronal mechanisms are identical for both NCSE and CSE, but they spare the primary motor neurons. Permanent hyperexcitability may damage the neurons involved in NCSE the same way as the motor neurons in CSE. However, NCSE is spared from the life-threatening secondary pathophysiological sequelae of CSE (lactic acidosis, respiratory exhaustion, rhabdomyolsis, etc.). Nevertheless, autonomic dysregulation (arrhythmias (ventricular tachycardia/asystolia), apneas) may also expose the patient to substantial acute risks. There are a myriad of causes for NCSE and they are mainly medication errors (insufficient adherence or addition of new drugs with interactions) in patients with known epilepsy. In these patients and in those without known epilepsy, other causes include metabolic, toxic, structural (tumors, hemorrhages, ischemia), infectious, inflammatory, and autoimmune causes. Thus, it is germane to extensively search for the cause of the NCSE because the immediate and proper therapy of the underlying cause of, especially the acute symptomatic, forms of NCSE is at least as important as the antiictal treatment.
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Özsoy, Sait, Hanife Alkurt Alkan, Sultan Pehlivan, Asude Gökmen, Ramazan Akçan, and Metin Alkan. "Death due to Aortobronchial Fistula Related Massive Hemoptysis a Case Report." Bulletin of Legal Medicine 21, no. 1 (April 1, 2016): 43–46. http://dx.doi.org/10.17986/blm.2016116600.
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Aortobronchial fistulas are relatively rare but usually fatal if not treated since they might cause massive hemoptysis. Here we present a case of death of a 17-year-old male due to massive hemoptysis secondary to aortobronchial fistula. The deceased was firstly admitted to an emergency department with dyspnea, tachypnea, tachycardia, resistant metabolic acidosis, confusion, and somnolence. He was diagnosed with “diabetic ketoacidosis” following examinations; however, detailed radiological and clinical investigations revealed community-acquired infection findings and medical treatment was started accordingly. He was discharged after 15 days of hospitalization; however, he died unexpectedly 12 days after discharge.At autopsy a 4-cm aortobronchial fistula was found between the thoracic aortic wall and the left main bronchus. Histopathological examination of fistula showed diffuse and intense necro-inflammatory reaction and inflammatory response with polymorphonuclear leukocytes and necrosis. Death was attributed to massive hemoptysis and blood aspiration due to aortobronchial fistula.A feedback system, towards healthcare centers, based on autopsy findings and exact cause and mechanisms of death will contribute improvement of diagnosis and treatment approach.Keywords: Aortopulmonary fistula; Respiratory Tract Fistula; Bronchial Fistula; Vascular Fistula; Hemoptysis; Cannabinoids; Autopsy.
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TakallooBakhtiari, Asieh, Julio Piedra Butina, Sheri A. Gillis Funderburk, and Hari V. Brundavanam. "Euglycemic DKA Associated With SGLT2 Inhibitors." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A382. http://dx.doi.org/10.1210/jendso/bvab048.778.
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Abstract Background: DKA associated with SGLT2 inhibitors also known as Euglycemic DKA (EDKA) is a rare condition characterized by milder degrees of hyperglycemia with a blood glucose level < 200 mg/dl. Unfortunately, this unusual feature can often lead to missed or delayed diagnosis with potential life-threatening outcomes. Clinical Case: The patient is a 53-year-old Caucasian male with PMH of type 2 diabetes mellitus treating with Metformin and Empagliflozin. He presented to the emergency room with shortness of breath, flu-like symptoms, and decreased oral intake for a couple of days. Vital signs at presentation were: Temperature 98.2 °F, pulse rate 108 beats/min, respiratory rate 28 breaths/min, and blood pressure 134/72 mmHg. He was alert but ill-looking, moderately dehydrated with dry mucus membranes. The rest of the physical examination was unremarkable at the time of admission. In the initial blood work, sugar was found to be mildly elevated (163mg/dl), and hemoconcentration besides mild pre-renal acute kidney injury was detected. He was also found infected by the COVID-19 virus without hypoxemia or signs of pneumonia. Arterial blood gases showed metabolic acidosis with an elevated anion gap (PH 7.21, CO2 39.93mmHg, HCO3− 10mEq/L, anion gap 21mEq/L). Urine analysis was positive for ketones and glucose. After ruling out other causes of metabolic acidosis by screening for alcohols, salicylates, acetaminophen, lactic acid, and urine toxicology; the diagnosis of EDKA was made. He was treated with a 3L bolus of IV normal saline and an insulin drip with dextrose solution started as per the protocol based on his glucose levels and promptly admitted to the intensive care unit (ICU). Serial blood tests showed gradual resolution of ketoacidosis and anion gap normalized after 36 hours when insulin drip was stopped and replaced by subcutaneous insulin therapy. Conclusion: SGLT2 inhibitors increase the urinary excretion rate of glucose and subsequent fall in plasma glucose level. Thus, In the absence of exogenous insulin use, increase glucagon release resulting in upregulation of lipolysis and activation of the ketogenesis. Factors such as low oral intake, concurrent infection, and alcohol use can also exacerbate the process. Timely diagnosis of EDKA can be a challenge for physicians unfamiliar with this class of medications, additionally, ketone studies and blood gas analyses are not part of the routine workup for diabetic patients in the emergency department. We recommend all first-line care providers to consider ketosis in ill patients with diabetes and metabolic acidosis, despite the normal or near-normal serum glucose levels. EDKA is mainly a diagnosis of exclusion, but treatment is not different from DKA; correcting dehydration by using intravenous fluids and then, initiating insulin drip along with dextrose-containing solutions, and frequent monitoring of serum anion gap.
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Yoshimi, Ayami, Sarah C. Grünert, Holger Cario, Ute Gross-Wieltsch, Udo Kontny, Kyogo Suzuki, Stephan Lobitz, et al. "Hematological Presentation and Change in Clinical Phenotype during Follow-up in Pearson Syndrome." Blood 134, Supplement_1 (November 13, 2019): 3746. http://dx.doi.org/10.1182/blood-2019-125199.
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Introduction: Pearson syndrome (PS) was originally reported as a sideroblastic anemia in infancy with vacuolization of marrow precursors and exocrine pancreas dysfunction. It is now recognized as a fatal multisystem mitochondrial disorder caused by single mitochondrial DNA deletions (SLSMDs) presenting with anemia. PS, Kearns-Sayre Syndrome (KSS) and progressive external ophthalmoplegia (PEO) form a continuous spectrum of disease associated with SLSMDs. There have been only a few systematic studies on PS. Methods: We retrospectively reviewed hematological features and clinical course of 25 children with PS diagnosed between 1987 and 2019. Results: Patients presented with normo/macrocytic transfusion-dependent anemia (n=25), failure to thrive (n=3), diarrhea (n=1), acidosis (n=1) and/or omphalocele/esophageal atresia (n=1) at a median age of 5 (0-31) months. A median hemoglobin, platelet count and neutrophil count were 6.5 (1.9-9.8) g/dl, 104 (31-300) G/L, and 0.9 (0.1-2.4) G/L, respectively. Bone marrow (n=24) was normo- (n=15) or hypocellular (n=9). Vacuoles in erythroid and myeloid precursors were observed in all patients, but ring sideroblasts were present in only 16 of 23 patients examined. Morphology can resemble Diamond-Blackfan anemia (DBA) because of erythroid hypoplasia (15/21). Dysplastic features are often observed including micromegakaryocytes. Lactic acid was elevated in most patients examined (14/18). Exocrine pancreas insufficiency at diagnosis was documented in 5 patients only. The detection of SLSMDs confirmed the diagnosis of PS in all patients. The median age at the time of the last follow-up was 47 (7 - 183) months. Among 11 patients with hematological follow-up for more than 3 years after diagnosis, 8 had spontaneous resolution of anemia at a median age of 28 (12-67) months, and 3 died at the age of 3, 6 or 8 years without hematological recovery. Clinical course was highly heterogeneous and various organ dysfunctions appeared. Renal tubulopathy/Fanconi syndrome (n=7) and cardiomyopathy/arrhythmia (n=5) were often fatal complications which developed at the median age of 32 and 45 months, respectively. Failure to thrive/short stature (n=13) and muscle hypotonia (n=9) were commonly observed. Other complications included pancreas insufficiency (n=7), liver dysfunction (n=4), endocrine dysfunctions (n=7), hearing loss (n=1), ophthalmoplegia (n=1), retinitis pigmentosa (n=1), cataract (n=1), ataxia (n=2) and encephalopathy (n=1). Thirteen patients died of acute metabolic acidosis with/without other complications (n=7), arrhythmia (n=2), respiratory failure (n=3) and liver/renal failure (n=1) at the median age of 50 (14-183) months. Two patients developed KSS and PEO-like phenotypes at the age 92 months and 19 months, respectively. Summary: Anemia is generally the only presenting syndrome of PS. While the bone marrow morphology can resemble DBA or myelodysplastic syndrome, recognition of vacuolated myeloid/erythroid precursors lead to the correct diagnosis of PS in all cases. Other classical signs of PS, ring-sideroblasts and pancreas insufficiency, are often missing. Anemia spontaneously resolves in most patients surviving early childhood. However, PS is unexceptionally fatal (Figure), most patients succumb to metabolic acidosis and various forms of multi-organ failure. Since there is no effective therapy, the diagnosis of PS is one of the saddest news that pediatric hematologists have to break to parents of an anemic infant. Figure Disclosures Niemeyer: Celgene: Consultancy.
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Kaya, Aslihan Gürün, Aydin Çiledağ, Çetin Atasoy, and Demet Karnak. "Flexible bronchoscopy and mechanical ventilation in managing Mounier-Kuhn syndrome: a case report." Sao Paulo Medical Journal 136, no. 3 (April 20, 2017): 266–69. http://dx.doi.org/10.1590/1516-3180.20160336270117.
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ABSTRACT CONTEXT: Mounier-Kuhn syndrome is a rare congenital condition with distinct dilatation and diverticulation of the tracheal wall. The symptoms may vary and the treatment usually consists of support. CASE REPORT: The patient was a 60-year-old male with recurrent hospital admission. He was admitted in this case due to dyspnea, cough and sputum production. An arterial blood sample revealed decompensated respiratory acidosis with moderate hypoxemia. A chest computed tomography (CT) scan showed dilatation of the trachea and bronchi, tracheal diverticula and bronchiectasis. Flexible bronchoscopy was performed, which revealed enlarged airways with expiratory collapse. Furthermore, orifices of tracheal diverticulosis were also detected. Non-invasive positive pressure ventilation (NPPV) was added, along with long-term oxygen therapy. At control visits, the patient’s clinical and laboratory findings were found to have improved. CONCLUSION: Flexible bronchoscopy can be advocated for establishing the diagnosis and non-invasive mechanical ventilation can be used with a high success rate, for clinical wellbeing in Mounier-Kuhn syndrome.
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Nazneen, Suraiya, Fatema Ahmed, SM Ashrafuzzaman, Khwaja Nazim Uddin, ASM Areef Ahsan, Mohammad Omar Faruq, Kaniz Fatema, Debasish Kumar Saha, Madhurima Saha, and Kamrul Hasan Sohel. "Clinical Presentation and Biochemical Abnormalities in Patients Presented with Diabetic Ketoacidosis in BIRDEM Hospital." Bangladesh Critical Care Journal 5, no. 1 (May 11, 2017): 7–10. http://dx.doi.org/10.3329/bccj.v5i1.32535.
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Objective: To see the clinical presentation and biochemical abnormalities in hospitalized patients of Diabetic ketoacidosis.Methodology: This cross sectional observational study was carried enrolling 55 subjects with Diabetic ketoacidosis, in the Department of Medicine, BIRDEM General Hospital, Dhaka, over a period of six months starting from April 2013 to September 2013.Results: The mean age was 48.35±16.76 with age range from 30 to 68 years. Infection (pneumonia, urinary tract infection, cellulitis) 22(40%), omission of insulin or drugs 14 (25.4%), myocardial infarction 5(9.0%), and reduction of insulin dose 3(5.4%) worked as precipitating cause.Most patients had drowsiness 16(29.0%), moderate dehydration 30(55.5%), signs of infection 22(40%). About 13(23.56%) had Kussmauls type of respiratory pattern. Other signs were less obvious. Majority of the subjects 40(72.7%) had 3+ ketonuria at the time of admission in hospital. About 32(58.1%) of the known diabetic patients were on insulin from the beginning of their diagnosis.19 (34.4%) were initially on OHA followed by insulin and 14 (25.4%) patients took OHA alone.7 patients were on dietary modification and exercise without any drugs. Majority 52 (96.46%) patients had blood sugar level between 21-34 mmol/l and mean HbA1c was 12.31(SD±2.50).About 4(7.2%) patients had severe hyponatraemia and 22(40%) patients had hypokalaemia. Eight (14.5%) patients had severe acidosis while 18(32.7%) patients had only mild acidosis. Most of the subjects 29(52.7%) had moderate acidosis. Complete cure from DKA was observed in 53(96.3%) subjects. Only 2(3.6%) subjects developed cerebral oedema. It took 4 to 5 days in mild group, 6 to 8 days in moderate DKA and more than 9 days in severe DKA for recovery.Conclusion: From the study result it could be concluded that infection control and regular administration of insulin or control of diabetes and proper Diabetes Self Management Education (DSME) can prevent diabetic ketoacidosis.Bangladesh Crit Care J March 2017; 5(1): 7-10
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Donati, Pablo, Leonel A. Londoño, Rodrigo Fravega, and Juan M. Guevara. "Successful resolution of urothorax secondary to non-traumatic uroabdomen in a cat managed with peritoneal dialysis as a bridge to surgery." Journal of Feline Medicine and Surgery Open Reports 7, no. 1 (January 2021): 205511692098474. http://dx.doi.org/10.1177/2055116920984748.
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Case summary A 9-year-old neutered male domestic shorthair cat was presented for evaluation of severe hemodynamic collapse and suspected lower urinary tract disease. On admission, severe metabolic acidosis, hyperkalemia and azotemia, and electrocardiographic findings consistent with cardiotoxicity were identified. The diagnosis of uroabdomen was made based on abdominal fluid to plasma concentration ratios of creatinine and potassium. A central line catheter was placed percutaneously into the abdomen for peritoneal drainage and used for peritoneal dialysis as a bridge to surgery. Retrograde contrast cystography confirmed rupture of the urinary bladder. Point-of-care ultrasound of the chest postoperatively revealed the presence of mild pleural effusion. Echocardiography was then performed showing no evidence of cardiac disease. Pleural fluid analysis revealed a transudate with a creatinine ratio of 2.38 ([Creatinine]pleural fluid/[Creatinine]plasma), consistent with the diagnosis of urothorax. The cat recovered uneventfully from surgery and was monitored for signs of respiratory distress during the rest of its stay in hospital. The cat was discharged 4 days later and the pleural effusion resolved without further medical intervention. Relevance and novel information There is limited information on the causes of urothorax and uroabdomen management of feline patients. Pleural effusion is a complication observed in critically ill cats secondary to fluid overload, underlying cardiomyopathy, primary thoracic pathology or a combination of these. To our knowledge, this is the first report of urothorax in a cat secondary to non-traumatic uroabdomen. Careful monitoring of respiratory signs consistent with pleural space disease is recommended in cases of uroabdomen.
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Kascak, Jelena, and Sladjana Andjelic. "Pickwickian syndrome - "the tip of the iceberg" in extremely obese patients." Srpski arhiv za celokupno lekarstvo 148, no. 3-4 (2020): 211–15. http://dx.doi.org/10.2298/sarh190222130k.
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Introduction. Pickwickian syndrome (PS), also known as hypoventilation syndrome in adults, consists of three factors: obesity [Body Mass Index (BMI) > 30 kg/m2], daytime hypercapnia and sleep-disordered breathing, after ruling out other disorders that may cause alveolar hypoventilation. Timely recognition of PS is of utmost importance because such patients have significant morbidity and mortality. However, recent data indicate that PS is under-recognized and under-treated. We report a case of early-identified PS prehospitally with a favorable outcome after hospital treatment. Case outline. A 67-year-old female patient was diagnosed prehospitally, and the diagnosis was later confirmed in hospital. Diagnostic criteria were as follows: BMI > 45,7 kg/m2 (height 170 cm, weight 132 kg), hypercapnia, hypoxemia and respiratory acidosis (pCO2 ? 41 mmHg, pO2 ? 56 mmHg, pH 7.45) in the absence of other causes of hypoventilation. During hospitalization, the following diagnostic procedures were performed: standard laboratory analyses, chest radiography, electrocardiography, abdomen and heart echocardiography. An attempted sleep study (polysomnography) was interrupted due to a drop in oxygen saturation levels. Non-invasive mechanical ventilation and a diet were used as the first line of therapy. However, due to the development of a global respiratory insufficiency, the patient was intubated and placed on a mechanical ventilator. After 30 days of hospital treatment, the patient was released in a satisfactory general condition with recommendations for weight reduction and symptomatic therapy. Conclusion. As obesity is becoming an epidemic of modern society, early recognition and treatment of PS is of crucial importance.
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Medina, G., D. González-Pérez, C. Vázquez-Juárez, M. Sánchez-Uribe, M. A. Saavedra, and L. J. Jara. "Fulminant systemic vasculitis in systemic lupus erythematosus. Case report and review of the literature." Lupus 23, no. 13 (August 8, 2014): 1426–29. http://dx.doi.org/10.1177/0961203314546018.
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Vasculitis in systemic lupus erythematosus (SLE) has a broad spectrum of clinical manifestations from cutaneous to visceral involvement and its prognosis ranges from mild to life-threatening. We report the case of a previously healthy 17-year-old woman with eight months' history of arthralgias and myalgias. Subsequently, she developed facial and lower limbs edema, and hair loss. Two weeks before admission to a secondary level hospital, she developed fever up to 40 ℃ followed by abdominal pain, rectal bleeding, hematemesis and blisters on both legs, reason for which she was hospitalized. With active bullous SLE with rapidly progressive glomerulonephritis suspected, she was treated with methylprednisolone pulses without response. After one week of treatment, she was transferred to a tertiary level hospital. On admission she presented acute arterial insufficiency of the lower extremities, respiratory failure with apnea, metabolic acidosis and shock; six hours later she died. Autopsy findings showed active diffuse lupus nephritis and diffuse systemic vasculitis that involved vessels from the skin, brain, myocardium, spleen, iliac and renal arteries. In addition, serositis of the small intestine and colon, acute and chronic pericarditis, pericardial effusion and myocarditis were found. Immunologic tests confirmed SLE diagnosis. In this case the fulminant course was the result of SLE high disease activity, visceral vasculitis of several organs and late diagnosis, referral and treatment. Early diagnosis, and opportune referral to the rheumatologist for intensive treatment can improve the outlook in these patients.
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Stevanus Eliansyah Handrawan, Mayang Indah Lestari, and Zulkifli. "Herbicide Intoxication : Still A Threat In Developing Countries." Journal of Anesthesiology and Clinical Research 1, no. 1 (June 20, 2020): 31–42. http://dx.doi.org/10.37275/jacr.v1i1.197.
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ABSTRACT
The critically ill patient has severe respiratory, cardiovascular or neurological disorder often in combination. The critically ill patient needs intensive care unit (ICU) admission and strict monitoring. Intoxication commonly experienced in a critically ill patient in ICU and can complicate management. In developing countries, poisoning of herbicide still common and used for suicide attempts. Herbicides such as paraquat and glyphosate are often used because of their availability. Paraquat and glyphosate have high mortality rate primarily as a suicide attempt agent in developing countries. The primary target for paraquat toxicity is in the lung and can cause lung fibrosis. Severe glyphosate intoxication can cause dehydration, hypotension, pneumonitis, oliguria, loss of consciousness, liver dysfunction, acidosis, hyperkalemia and dysrhythmia. Diagnosis for herbicide intoxication needs a history of herbicide ingestion, physical examination and laboratory examination. Stabilisation and supportive therapy is the only choice, and there is still no specific treatment for herbicide intoxication. The intoxication of herbicide particular critically ill patient because there is still no such specific treatment for these.