scholarly journals Is severe hypocalcemia immediately life threatening?

2018 ◽  
Vol 7 (10) ◽  
pp. 1067-1074 ◽  
Author(s):  
Maxime Duval ◽  
Kalyane Bach-Ngohou ◽  
Damien Masson ◽  
Camille Guimard ◽  
Philippe Le Conte ◽  
...  

Objective Severe hypocalcemia (Ca <1.9 mmol/L) is often considered an emergency because of a potential risk of cardiac arrest or seizures. However, there is little evidence to support this. The aim of our study was to assess whether severe hypocalcemia was associated with immediately life-threatening cardiac arrhythmias or neurological complications. Methods A retrospective observational study was carried out over a 2-year period in the Adult Emergency Department (ED) of Nantes University Hospital. All patients who had a protein-corrected calcium concentration measure were eligible for inclusion. Patients with multiple myeloma were excluded. The primary outcome was the number of life-threatening cardiac arrhythmias and/or neurological complications during the stay in the ED. Results A total of 41,823 patients had protein-corrected calcium (pcCa) concentrations measured, 155 had severe hypocalcemia, 22 were excluded because of myeloma leaving 133 for analysis. Median pcCa concentration was 1.73 mmol/L (1.57–1.84). Seventeen (12.8%) patients presented a life-threatening condition, 14 (10.5%) neurological and 3 (2.2%) cardiac during ED stay. However, these complications could be explained by the presence of underlying co-morbidities and or electrolyte disturbances other than hypocalcemia. Overall, 24 (18%) patients died in hospital. Vitamin D deficiency, chronic kidney disease and hypoparathyroidism were the most frequently found causes of hypocalcemia. Conclusion Thirteen percent of patients with severe hypocalcemia presented a life-threatening cardiac or neurological complication on the ED. However, a perfectly valid alternative cause could account for these complications. Further research is warranted to define the precise role of hypocalcemia.

Author(s):  
Stefano Sartini ◽  
Laura Massobrio ◽  
Ombretta Cutuli ◽  
Paola Campodonico ◽  
Cristina Bernini ◽  
...  

COVID-19 respiratory failure is a life-threatening condition. Oxygenation targets were evaluated in a non-ICU setting. In this retrospective, observational study, we enrolled all patients admitted to the University Hospital of Genoa, Italy, between 1 February and 31 May 2020 with an RT-PCR positive for SARS-CoV-2. PaO2, PaO2/FiO2 and SatO2% were collected and analyzed at time 0 and in case of admission, patients who required or not C-PAP (groups A and B) were categorized. Each measurement was correlated to adverse outcome. A total of 483 patients were enrolled, and 369 were admitted to hospital. Of these, 153 required C-PAP and 266 had an adverse outcome. Patients with PaO2 <60 and >100 had a higher rate of adverse outcome at time 0, in groups A and B (OR 2.52, 3.45, 2.01, respectively). About the PaO2/FiO2 ratio, the OR for < 300 was 3.10 at time 0, 4.01 in group A and 4.79 in group B. Similar odds were found for < 200 in any groups and < 100 except for group B (OR 11.57). SatO2 < 94% showed OR 1.34, 3.52 and 19.12 at time 0, in groups A and B, respectively. PaO2 < 60 and >100, SatO2 < 94% and PaO2/FiO2 ratio < 300 showed at least two- to three-fold correlation to adverse outcome. This may provide simple but clear targets for clinicians facing COVID-19 respiratory failure in a non ICU-setting.


Author(s):  
Linda Bāra ◽  
Jeļena Eglīte ◽  
Pēteris Ošs ◽  
Vinita Cauce ◽  
Vilnis Lietuvietis ◽  
...  

Abstract Undeniably, sepsis is still a profoundly damaging and life-threatening condition for many individuals. With multiple changes in sepsis patients it is difficult to precisely classify an individual’s response in sepsis as proinflammatory or immunosuppressed. The aim of this study was to investigate genetically determined predisposition to developed sepsis by analysis of distribution of human leukocyte antigen (HLA) class II genes. Samples from patients with sepsis were collected at Pauls Stradiņš Clinical University Hospital, Latvia, in an intensive care unit between October 2016 and May 2017. The study group included 62 patients with sepsis, who were genotyped for HLA-DR; DQ using real time polymerase chain reaction – sequence specific primer (RT PCR-SSP). As a control group, data of 100 individuals were taken from the genetic bank of RSU Joint Laboratory of Clinical Immunology and Immunogenetics. The summarised results showed that the frequency of alleles DRB1*04:01 (OR = 5.54; 95% CI = 1.88–16.29); DRB1*07:01 (OR = 19.03; 95% CI = 2/37–152.82); DQA1*05:01 (OR = 14.17; 95% CI = 5.67–35.4); and DQB1*02:01 (OR = 50.00; 95% CI = 2.90–861.81) were significantly increased in patients with sepsis compared to the control group patients. The frequency of DRB1*16:01 (OR = 0.17, 95% CI = 0.04–0.59); DRB1*17:01 (OR = 0.04; 95% CI = 0.00–0.69); DQA1*01:01 (OR = 0.04; 95% CI = 0.00–0.31); DQA1*01:02 (OR = 0.03; 95% CI = 0.00–0.23); DQB1*02:02 (OR = 0.12; 95% CI = 0.03–0.42) alleles was lower in sepsis patients than in control subjects. The most frequent HLA-DRB1/DQA1/DQB1 haplotypes that was significantly increased in patients with sepsis were: DRB1*01:01/DQA1*05:01/DQB1*03:01 (OR = 12.6; 95% CI = 1.51–105.0; p < 0.003). Sepsis patients with pneumonia and alleles and DRB1 04:01; 07:01, DQB1 02:01 had the highest mortality rate. Undoubtedly, our preliminary data showed that development of sepsis can be associated with alleles and haplotypes of HLA class II genes. For more precise conclusion the research should be continued to include a larger patient group.


2020 ◽  
Vol 88 (4) ◽  
pp. 189-191
Author(s):  
Nagendra Singh Sonwani ◽  
Navneet Ateriya ◽  
Arvind Kumar ◽  
Anil Kohli ◽  
Kalyan Kumar Banerjee

Acute haemorrhage from ruptured oesophageal varices is a serious consequence of portal hypertension in cirrhotic patients. It represents a medical emergency with a high morbidity and mortality rate. Studies over the years have shown a direct link with chronic alcoholism in the development of such complications. Although the gastrointestinal system accounts for a few numbers of sudden deaths, bleeding through ruptured varices represent a life-threatening condition. The role of forensic pathologist is vital in dealing with sudden deaths. Here, we report a case of a 46-year-old man who died suddenly following the rupture of oesophageal varices.


2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Gregory C. Davenport ◽  
James B. Hittner ◽  
Vincent Otieno ◽  
Zachary Karim ◽  
Harshini Mukundan ◽  
...  

Bacteremia and malaria coinfection is a common and life-threatening condition in children residing in sub-Saharan Africa. We previously showed that coinfection with Gram negative (G[−]) enteric Bacilli andPlasmodium falciparum(Pf[+]) was associated with reduced high-density parasitemia (HDP, >10,000 parasites/μL), enhanced respiratory distress, and severe anemia. Since inflammatory mediators are largely unexplored in such coinfections, circulating cytokines were determined in four groups of children (n=206, aged <3 yrs): healthy;Pf[+] alone; G[−] coinfected; and G[+] coinfected.Staphylococcus aureusand non-TyphiSalmonellawere the most frequently isolated G[+] and G[−] organisms, respectively. Coinfected children, particularly those with G[−] pathogens, had lower parasite burden (peripheral and geometric mean parasitemia and HDP). In addition, both coinfected groups had increased IL-4, IL-5, IL-7, IL-12, IL-15, IL-17, IFN-γ, and IFN-αand decreased TNF-αrelative to malaria alone. Children with G[−] coinfection had higher IL-1βand IL-1Ra and lower IL-10 than thePf[+] group and higher IFN-γthan the G[+] group. To determine how the immune response to malaria regulates parasitemia, cytokine production was investigated with a multiple mediation model. Cytokines with the greatest mediational impact on parasitemia were IL-4, IL-10, IL-12, and IFN-γ. Results here suggest that enhanced immune activation, especially in G[−] coinfected children, acts to reduce malaria parasite burden.


2020 ◽  
Vol 116 (9) ◽  
pp. 1600-1619 ◽  
Author(s):  
Ali J Marian ◽  
Babken Asatryan ◽  
Xander H T Wehrens

Abstract Cardiac arrhythmias are common, often the first, and sometimes the life-threatening manifestations of hereditary cardiomyopathies. Pathogenic variants in several genes known to cause hereditary cardiac arrhythmias have also been identified in the sporadic cases and small families with cardiomyopathies. These findings suggest a shared genetic aetiology of a subset of hereditary cardiomyopathies and cardiac arrhythmias. The concept of a shared genetic aetiology is in accord with the complex and exquisite interplays that exist between the ion currents and cardiac mechanical function. However, neither the causal role of cardiac arrhythmias genes in cardiomyopathies is well established nor the causal role of cardiomyopathy genes in arrhythmias. On the contrary, secondary changes in ion currents, such as post-translational modifications, are common and contributors to the pathogenesis of arrhythmias in cardiomyopathies through altering biophysical and functional properties of the ion channels. Moreover, structural changes, such as cardiac hypertrophy, dilatation, and fibrosis provide a pro-arrhythmic substrate in hereditary cardiomyopathies. Genetic basis and molecular biology of cardiac arrhythmias in hereditary cardiomyopathies are discussed.


2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 136-136
Author(s):  
Sanjeev Parshad ◽  
Parvinder Sandu ◽  
Shekar Gogna ◽  
Abhijeet Beniwal ◽  
Rajendra Karwasra

Abstract Background Chyle leak after esophagectomy for carcinoma esophagus is a rare but life threatening condition with reported an incidence of 1–6%. Mortality rate of up to 50% have been reported. Management of chyle leak is controversial. We reviewed our experience with iatrogenic chylothorax after esophagectomy for carcinoma esophagus. Methods From 2003 to 2017, 560 patients underwent esophagectomy for cancer at our department of oncosurgery. Eight patients developed post operative chyle leak. Transthoracic or transabdominal ligation of duct was done in six patients with in first week. 100 ml of cream was given 30 min before induction to visualize the leak intraoperatively. We used 4–0 prolene pledgeted suture to ligate the duct. Results Six patients who underwent early ligation could be salvaged and the two who were managed conservatively succumbed. Oringer et al. pointed towards conservative treatment having little place in the management of chylothorax in nutritionally depleted patients. Hence, prompt ligation of thoracic duct decreases morbidity and mortality of chylothorax. Thus the role of early surgery needs to stressed. There is a wide difference of mortality rate of conservative management of 82% with respect to the mortality rate of surgery of 10–16%. Though no conclusion data are available regarding the indication and time point of surgical ligation of the thoracic duct, it is important not to procrastinate while the condition deteriorates to a level at which surgery would be detrimental.Administration of cream to the patient (through feeding jejunostomy) around half an hour before surgery makes identification of site of leak simpler.The importance of pledgeted sutures cannot be denied as the thoracic duct is paper thin and chyle contains no fibrin. Thus non pledgeted sutures will tear it further. Infact, stitching should not be done through the duct but into the surrounding tissue around the duct and should allow the pledgets to close the duct. Conclusion Disclosure All authors have declared no conflicts of interest.


2020 ◽  
Vol 13 (4) ◽  
pp. e232411 ◽  
Author(s):  
Ugochukwu Chinyere Chinaka ◽  
Joshua Fultang ◽  
Jelizaveta Pereca ◽  
Abdulmajid Ali

Splenic rupture is a potentially life-threatening condition and an uncommon short-term complication of granulocyte-colony stimulating factor (G-CSF) administration. It may present as acute abdominal pain or suddenly precipitously worsening anaemia with haemodynamic instability that requires urgent operative intervention for survival. We present a case of an atraumatic idiopathic splenic rupture in University Hospital, Ayr in a patient who received G-CSF treatment for chemotherapy-induced (methotrexate) pancytopenia and was successfully managed by laparoscopic splenectomy.


2017 ◽  
Vol 16 (1) ◽  
pp. 186-186
Author(s):  
B.D. Sigmarsdottir ◽  
Th.K. Gudmundsdottir ◽  
S. Zoäga ◽  
P.S. Gunnarsson

Abstract Aims Respiratory depression is a serious life threatening condition and a known adverse event of opioids. Little is known about the use of the opioid antidote naloxon in Iceland, and the additive effects of other potentially respiratory depressive drugs administered with opioids. The aim of the study was to review the literature on drugs that may cause respiratory depression and to assess medication use in patients receiving parenteral naloxone in Landspítali University Hospital. Methods A review and analysis of drugs that can cause respiratory depression based on information from the scientific literature, medicine databases and clinical guidelines. A retrospective study was performed using data collected from the electronic medical records system of Landspítali University Hospital for all patients, 18 years and older that had parenteral naloxon administered in the years 2010–2014. Information about the type of opioid and other respiratory depressive drugs was collected and the data was further investigated in regards to age, gender, and type of service. Results The most potential drugs and drug classes that can cause respiratory depression when used concomitantly with opioids are benzodiazepines and other anxiolytics, hypnotics and sedatives, antipsychotics, antiepileptics, antihistamins and anesthetics. When use was examined (N=138) morphine was the most frequent opioid given (49%). Concomitant use of opioids and other respiratory depressive drugs was seen in 63% of cases, and benzodiazepines were the most frequent drugs given with opioids (33%). Conclusions The concomitant use of benzodiazepines and other sedative drugs with opioids is frequent, despite the known risk of additive respiratory depression as described in the literature. Other patient risk factors such as medical condition, general health and consciousness should be considered in context with drugs used.


2016 ◽  
Vol 33 (S1) ◽  
pp. S631-S632 ◽  
Author(s):  
A. Gomez Peinado ◽  
P. Cano Ruiz ◽  
M.D. Sanchez Garcia ◽  
S. Cañas Fraile ◽  
M. Gonzalez Cano ◽  
...  

IntroductionNeuroleptic malignant syndrome (NMS) takes place in patients in treatment with neuroleptics and it is potentially lethal, being important an early diagnostic and therapeutic approach.ObjectivesTo analyze from a clinical case the clinical and epidemiological features, and therapeutical approach to NMS.MethodReview of some articles in Mental Health journals and analysis of the following clinical case: 68-year-old woman with bipolar disorder, hospitalized in manic phase. Usual treatment: lithium, trazodone, quetiapine and asenapine. During the admission to hospital, the patient started presenting hyperthermia, sweating, electrolyte disturbances, limb rigidity, and elevation of CPK levels. The suspicion was NMS, so neuroleptics were stopped and fluids and dantrolene were initiated, with favorable evolution.ResultsThe discharge diagnosis was NMS. Neuroleptics were gradually reintroduced under vigilance. The patient is stable and has not had new complications. NMS is an uncommon (0.02% to 3% among patients taking neuroleptic agents), but life-threatening condition. Its symptoms are hyperthermia, autonomic nervous system dysfunction, limb rigidity, altered consciousness… The attendant infections, consume of lithium, dehydration, iron deficiency and sharp changes in neuroleptic treatment are predisposing factors. The withdrawal of neuroleptics is the key of the treatment. Benzodiazepines can improve the prognosis, and electroconvulsive therapy can be necessary if there is no response to previous measures.ConclusionsNeuroleptic malignant syndrome is a life-threatening medical complication we should try to avoid by a correct and careful use of neuroleptics. Additionally, it is important the early treatment, taking withdrawal of neuroleptics as the key starting point.Disclosure of interestThe authors have not supplied their declaration of competing interest.


F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 62
Author(s):  
Ezza Fatima Tariq ◽  
Yusra Irshad ◽  
Usman A. Khan ◽  
Muhammad Shoaib ◽  
Hajra Asif

Voriconazole, an azole drug, inhibits cytochrome P450 dependent lanosterol 14-alpha-demethylase. It is a potent anti-fungal agent. Adverse effects include neurotoxicity, cardiac arrhythmias, electrolyte disturbances and adrenal insufficiency. Hyperkalemia is a rare adverse effect that has been described, but is not well reported, in the literature. We present a case of intractable hyperkalemia resulting from voriconazole use. A 47-year-old male presented with worsening shortness of breath, requiring mechanical ventilation within 24 hours of presentation. Diagnosis of acute respiratory distress syndrome was made. Empirical treatment with broad-spectrum antibacterial coverage resulted in no improvement. Voriconazole was added for anti-fungal coverage, causing treatment resistant hyperkalemia necessitating continuous renal replacement therapy (CRRT). Renal function remained normal. Stopping voriconazole restored normal potassium levels. CRRT was discontinued. Hyperkalemia caused by voriconazole occurs in less than 2% of cases. It is a potentially life-threatening side effect. Physicians should be aware of this association and seek alternative treatment when necessary.


Sign in / Sign up

Export Citation Format

Share Document