[Multiple organ failure in a severely malnourished patient with chromosome aberration]

Roman Kaźmirczuk1, Marlena Jakubczyk, Sylwia Kołtan

  • 1Oddział Kliniczny Anestezjologii i Intensywnej Terapii dla Dzieci Collegium Medium UMK w Bydgoszczy. kikanest@cm.umk.pl

Insights

Severe malnutrition in a disabled child led to multiple organ failure, highlighting the critical need for intensive care and specialized treatment for such complex pediatric cases.

Area of Science:

  • Pediatric critical care
  • Nutritional deficiencies
  • Genetics and chromosomal abnormalities

Background:

  • Pneumonia and malnutrition are leading causes of childhood mortality globally.
  • These conditions, though prevalent in developing nations, also affect children in developed countries due to neglect.
  • Severe malnutrition can precipitate multiple organ failure, even in non-developing settings.

Observation:

  • A 16-year-old female with a +14q chromosome aberration presented with severe anemia and dyspnea.
  • She exhibited extreme malnutrition (BMI 13.9), requiring intensive medical intervention.
  • Complications included transfusion-related acute lung injury (TRALI) and multiple organ failure.

Findings:

  • The patient experienced prolonged dysfunction of homeostasis, hypoproteinemia, hypophosphatemia, and systemic inflammatory response syndrome (SIRS).
  • Treatment involved mechanical ventilation, inotropic support, and parenteral nutrition, complicated by refeeding syndrome and gastrointestinal hemorrhage.
  • Surgical interventions, including gastrostomy and adhesiolysis, were necessary for recovery.

Implications:

  • This case underscores the severe consequences of prolonged malnutrition, particularly in intellectually disabled children.
  • Management of such complex cases requires meticulous care in intensive care unit (ICU) settings.
  • Highlights the challenges in treating malnutrition-induced organ failure and associated metabolic disturbances.
Abstract

Related Concept Videos

Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
Tissue Transplantation01:24

Tissue Transplantation

Tissue transplantation is a significant medical procedure involving the transfer of cells, tissues, or organs from a donor to a recipient, with the primary aim of restoring lost functions. This procedure is crucial in treating a broad spectrum of diseases, including kidney diseases, liver failure, heart disease, and certain types of cancers.
The Biology of Tissue Transplantation
The biology of tissue transplantation hinges on the Major Histocompatibility Complex (MHC) molecules. These molecules...
Overview of Protein Metabolism01:21

Overview of Protein Metabolism

Proteins are broken down into amino acids during digestion. Unlike fats and carbohydrates, which are stored for later use, proteins are not. Instead, amino acids are either used to produce ATP through oxidation or contribute to the creation of new proteins for the growth and repair of the body. Any surplus amino acids from the diet are converted into glucose or triglycerides rather than excreted.
Amino acids play various roles in the body once they are absorbed into cells. They are restructured...
Intestinal Obstruction II: Pathophysiology01:07

Intestinal Obstruction II: Pathophysiology

Intestinal obstruction triggers a series of physiological responses, starting with gas and fluid accumulation in the bowel segment proximal to the obstruction, leading to distension. This distended intestine compresses the diaphragm, hindering lung expansion and potentially leading to reduced respiratory effort, atelectasis, and pneumonia.To overcome the blockage, the gut intensifies contractions, causing colicky abdominal pain, nausea, and vomiting, which reduces fluid and food intake and...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...