Nitroglycerin reverts clinical manifestations of poor peripheral perfusion in patients with circulatory shock

Background:Severe malaria (SM) remains a major global health problem causing ~275,000 pediatric deaths annually, worldwide. Continuous, non-invasive monitoring of peripheral perfusion can help detect abnormalities in systemic circulation, a common problem in critically ill patients, and can improve outcomes in children hospitalized with SM. Perfusion index (PI), an indicator of peripheral perfusion measured using a point-of-care pulse oximeter, is the ratio of pulsatile blood flow to static blood in peripheral tissue. Objective: To investigate the role of PI as an indicator of adverse outcomes including mortality in children hospitalized with SM. Methods: We measured PI in a prospective cohort study of 600 children <5 years of age with 5 different clinical manifestations of SM, and 120 healthy community children (CC) at two hospitals in Uganda. PI was measured at 6-hr intervals during hospitalization using a Masimo Rad 57 pulse oximeter. Results: Children with SM had significantly lower admission PI values (1.2 [IQR: 0.58, 2.2] compared to CC (2.8 [1.7, 4.3], p<0.001). Children with SM manifesting as respiratory distress syndrome or severe malarial anemia had lower median PI compared to other manifestations including cerebral malaria, the deadliest form of SM in children. In children with SM, a log decrease in admission PI was associated with 2.7 higher odds of in-hospital mortality (p=0.01). A log reduction in PI was also associated with in-hospital clinical complications associated with SM, including circulatory shock, deep acidotic breathing and acidosis, hypoglycemia, and severe anemia (all P<0.03). In survivors of SM, there were no significant associations between PI and cognitive outcomes at 12-month follow-up. Conclusion: The role of PI as an indicator of mortality in children with SM and the use of point-of-care tools for continuous monitoring of PI warrants further investigation in the management of SM to prevent or reduce the incidence of adverse outcomes.

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Intravenous Insulin Resistance in a Critically Ill Patient Secondary to Decreased Peripheral Perfusion

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.791 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A388-A388

Author(s):

Deviani Umadat ◽

Dharscika Arudkumaran ◽

Deirdre Cocks Eschler

Keyword(s):

Aortic Valve ◽

Aortic Valve Replacement ◽

Insulin Infusion ◽

Regular Insulin ◽

Central Line ◽

Insulin Requirement ◽

Peripheral Perfusion ◽

Insulin Requirements ◽

Central Access ◽

Poor Peripheral Perfusion

Abstract Introduction: Intravenous (IV) insulin infusion is the preferred treatment modality for hyperglycemia in the intensive care unit (ICU) due to its short duration of action and easy titratability. However, administration of IV insulin has challenges. These include frequent monitoring, site infiltration, and high insulin dose requirements with other ICU medications such as epinephrine. There are, however, limited reports demonstrating an elevated insulin requirement due to poor peripheral perfusion. Below illustrates such a case, necessitating a change from peripheral to central IV insulin administration. Case Presentation: A 50 year old male with well controlled type 2 diabetes and previous aortic valve replacement presented to our facility for prosthetic valve endocarditis complicated by aortic root abscess. He was admitted to the ICU, treated with IV antibiotics, abscess washout and aortic valve replacement. Preoperatively, he was started on IV regular insulin via continuous infusion through a central line. During the pre and intraoperative periods, his hourly IV insulin requirement ranged from 2.4 to 5 units/ hour (hr). His blood glucose (BG) ranged from 107-251mg/dL (n 70-99mg/dL). The patient became hypotensive intraoperatively requiring vasopressor support. Dobutamine and norepinephrine infusions were started via central access and were continued postoperatively at steady rates. Vasopressin was added through central access as the patient failed to meet hemodynamic targets. Postoperatively, the propofol infusion was discontinued and the IV regular insulin infusion was moved to the peripheral line where the propofol had previously been administered. BG increased steadily to a maximum of 402 mg/dL despite an increase in the peripheral IV insulin rate to 152.4 units/hr. The site of the IV insulin drip was changed to another solitary peripheral access without success in decreasing the IV insulin infusion rate. The elevated requirements were deemed secondary to the patient’s lack of peripheral perfusion and should decrease with transition to a central line. A preemptive decrease in insulin drip rate to 10% of the peripheral dose was used to avoid hypoglycemia. The insulin drip was changed to a central access with a rate of 15units/ hr. BG values declined to a range of 140 -180 mg/dL. The patient remained on the multiple vasopressors for hemodynamic support, however, the insulin drip was able to be decreased and ultimately, discontinued. Conclusion: This case illustrates a unique challenge in the treatment of hyperglycemia with multifactorial shock and our approach to management. Elevated IV insulin requirements persisted despite stability in vasopressor dose, change to a solitary peripheral IV site, and lack of interfering medications in the treatment regimen. This is the first case to demonstrate a relationship between high IV insulin requirements and poor peripheral perfusion.

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Morphologic alteration in the muscles of patients with hypokalemic periodic paralysis or myopathy

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100158650 ◽

1990 ◽

Vol 48 (3) ◽

pp. 222-223

Author(s):

T. Shimizu ◽

Y. Muranaka ◽

I. Ohta ◽

N. Honda

Keyword(s):

Clinical Manifestations ◽

Quadriceps Muscle ◽

Honeycomb Structure ◽

Periodic Paralysis ◽

Ultrastructural Changes ◽

Hypokalemic Periodic Paralysis ◽

Electron Microscopic ◽

Tubular Aggregates ◽

Hypokalemic Myopathy ◽

Transmission Electron

There have been many reports on ultrastructural alterations in muscles of hypokalemic periodic paralysis (hpp) and hypokalemic myopathy(hm). It is stressed in those reports that tubular structures such as tubular aggregates are usually to be found in hpp as a characteristic feature, but not in hm. We analyzed the histological differences between hpp and hm, comparing their clinical manifestations and morphologic changes in muscles. Materials analyzed were biopsied muscles from 18 patients which showed muscular symptoms due to hypokalemia. The muscle specimens were obtained by means of biopsy from quadriceps muscle and fixed with 2% glutaraldehyde (pH 7.4) and analyzed by ordinary method and modified Golgimethod. The ultrathin section were examined in JEOL 200CX transmission electron microscopy.Electron microscopic examinations disclosed dilated t-system and terminal cistern of sarcoplasmic reticulum (SR)(Fig 1), and an unique structure like “sixad” was occasionally observed in some specimens (Fig 2). Tubular aggregates (Fig 3) and honeycomb structure (Fig 4) were also common characteristic structures in all cases. These ultrastructural changes were common in both the hypokalemic periodic paralysis and the hypokalemic myopathy, regardless of the time of biopsy or the duration of hypokalemia suffered.

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Clinical manifestations and complications of childbirth and replacement therapy in 385 Iranian patients with type 3 von Willebrand disease

British Journal of Haematology ◽

10.1046/j.1365-2141.2000.02507.x ◽

2000 ◽

Vol 111 (4) ◽

pp. 1236-1239 ◽

Cited By ~ 129

Author(s):

M. Lak ◽

F. Peyvandi ◽

P. M. Mannucci

Keyword(s):

Replacement Therapy ◽

Clinical Manifestations ◽

Von Willebrand Disease ◽

Type 3 ◽

Von Willebrand ◽

Iranian Patients

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446 Predictors of clinical manifestations and courses in patients with acute fulminant coxsackievirus myocarditis

European Journal of Heart Failure Supplements ◽

10.1016/s1567-4215(05)80287-5 ◽

2005 ◽

Vol 4 (1) ◽

pp. 104-104

Keyword(s):

Clinical Manifestations

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The sickle cell diseases. Clinical manifestations including the "sickle crisis"

Archives of Internal Medicine ◽

10.1001/archinte.133.4.611 ◽

1974 ◽

Vol 133 (4) ◽

pp. 611-619 ◽

Cited By ~ 14

Author(s):

F. I. Konotey-Ahulu

Keyword(s):

Sickle Cell ◽

Clinical Manifestations

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Nutritional B12 Deficiency in Infants of Vitamin B12-Deficient Mothers

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000080 ◽

2011 ◽

Vol 81 (5) ◽

pp. 328-334 ◽

Cited By ~ 6

Author(s):

Oya Halicioglu ◽

Sezin Asik Akman ◽

Sumer Sutcuoglu ◽

Berna Atabay ◽

Meral Turker ◽

...

Keyword(s):

Megaloblastic Anemia ◽

Maternal Diet ◽

Clinical Manifestations ◽

Serum Vitamin ◽

Failure To Thrive ◽

Clinical Findings ◽

Vitamin B ◽

Animal Products ◽

Hematological Evaluation ◽

Nutritional Vitamin

Aim: Nutritional vitamin B12 deficiency in infants may occur because the maternal diet contains inadequate animal products. Clinical presentations of the infants who had nutritional vitamin B12 deficiency were analyzed in this study. Subjects and Methods: Patients with nutritional vitamin B12 deficiency were enrolled in the study between 2003 and 2010. The diagnosis was based on a nutritional history of mothers and infants, clinical findings, hematological evaluation, and low level of serum vitamin B12. Results: Thirty children aged 1 - 21 months constituted the study group. Poverty was the main cause of inadequate consumption of animal products of the mothers. All infants had predominantly breastfed. The most common symptoms were developmental delay, paleness, apathy, lethargy, anorexia, and failure to thrive. Hematological findings were megaloblastic anemia (83.3 %), thrombocytopenia (30 %), and severe anemia (13.3 %). All of the mothers had low serum B12 levels; eight of them had megaloblastic anemia. Conclusion: The unusual clinical manifestations of vitamin B12 deficiency may also be seen apart from neurological and hematological findings. Nutritional vitamin B12 deficiency due to maternal deficiency might be a serious health problem in infants. Therefore, screening and supplementation of pregnant and lactating women to prevent infantile vitamin B12 deficiency should be considered.

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