Showing posts with label Pathophysiology. Show all posts
Showing posts with label Pathophysiology. Show all posts

Friday, September 06, 2024

EMS Airway Emergencies - Esophageal Varices


Esophageal Varices
are abnormally dilated veins in the lower part of the esophagus that develop as a result of portal hypertension, commonly due to liver cirrhosis. 

These varices pose a high risk of massive upper gastrointestinal (GI) bleeding, which can be life-threatening. 

When esophageal varices rupture, they can cause severe hematemesis (vomiting of blood), shock, and potentially death if not managed promptly.

Causes and Pathophysiology

- Portal Hypertension: The most common cause of esophageal varices is liver cirrhosis (often due to chronic alcohol use, hepatitis B or C, or fatty liver disease).

Portal hypertension occurs when the liver becomes scarred and obstructs blood flow, leading to increased pressure in the portal venous system.

- Collateral Circulation Formation: To relieve this increased pressure, the body forms collateral blood vessels (varices) in the esophagus and stomach. These varices are thin-walled and prone to rupture.

- Rupture and Hemorrhage: When pressure becomes too high or if the varices are mechanically disrupted (e.g., vomiting, coughing), they can rupture, leading to severe bleeding.

Signs and Symptoms of Esophageal Variceal Bleeding

EMS providers should be alert for the following symptoms in patients with a known history of liver disease or portal hypertension:

- Profuse Hematemesis: Patients often present with large volumes of bright red blood in vomit, which is the hallmark sign of a ruptured varix.

- Melena or Hematochezia: Blood may pass through the GI tract and present as black, tarry stools (melena) or bright red rectal bleeding (hematochezia), depending on the speed and severity of the bleed.

- Hypovolemic Shock: Tachycardia and hypotension are common signs. Cool, clammy skin, altered mental status, and pallor indicate worsening shock.

- Signs of Liver Disease: 

  • Jaundice (e.g., yellowing of the skin and eyes)
  • Ascites (e.g., swollen abdomen due to fluid accumulation)
  • Spider Angiomata (e.g., visible, web-like blood vessels on the skin)
  • Hepatic Encephalopathy (e.g., confusion, altered consciousness)

Prehospital Assessment

- Scene Size-Up and Initial Impression: Evaluate the scene for large amounts of blood, which can indicate massive hemorrhage.

Assess for a patient history of liver disease, alcoholism, or known cirrhosis.

- Airway & Breathing: Monitor for airway obstruction due to blood in the mouth or pharynx.

Be prepared to suction the airway frequently to prevent aspiration.

Assess respiratory status and provide high-flow oxygen if needed.

- Circulatory Assessment: Check for signs of shock (e.g., tachycardia, hypotension).

Establish large-bore IV access (18 gauge or larger) for potential fluid and medication administration.

Monitor mental status and skin condition (pallor, coolness).

- Focused History & Physical Exam: Ask about the patient’s history of liver disease, alcohol use, hepatitis, or prior variceal bleeding.

Inquire about recent triggers (e.g., vomiting, straining, recent alcohol binge) that may have precipitated bleeding.

Prehospital Treatment and Management

Managing esophageal varices in the prehospital setting is challenging and requires prompt, aggressive intervention to control bleeding and prevent shock.

1. Airway Management

- Suctioning: Keep a suction device readily available for continuous use to clear the airway of blood.

- Airway Positioning: Consider placing the patient in the left lateral recumbent position if unconscious to reduce the risk of aspiration.

- Definitive Airway: If the patient is at risk of losing their airway (e.g., massive hematemesis or altered mental status), consider early endotracheal intubation, if within your scope and if protocols allow.

2. Hemodynamic Support

- IV Fluid Resuscitation: Establish two large-bore IVs and begin fluid resuscitation with isotonic crystalloids (e.g., normal saline) if the patient shows signs of hypovolemic shock.

Avoid aggressive fluid overload, as it can increase portal hypertension and worsen bleeding.

- Blood Products: If available (e.g., in critical care transport), consider initiating blood transfusion early in patients with significant bleeding or hemorrhagic shock.

3. Medications

- Vasoactive Agents (for ALS Providers): If within your scope and protocol, consider octreotide or vasopressin, which can reduce portal pressure and control variceal bleeding (requires medical control consultation).

- Anti-Emetics: Administer antiemetics (e.g., ondansetron) to prevent retching and reduce the risk of worsening the variceal tear.

4. Rapid Transport and Early Notification

- Transport Priority: All patients with suspected variceal bleeding should be considered critical and require rapid transport to the nearest facility with endoscopic capabilities and surgical backup.

- Early Notification: Notify the receiving hospital as early as possible about the suspected diagnosis, so the facility can mobilize appropriate resources.

Differentiating from Other GI Bleeds

- Peptic Ulcer Disease: Often presents with coffee-ground emesis and less profuse bleeding.

- Mallory-Weiss Syndrome: Similar to varices but generally involves small, non-life-threatening mucosal tears with moderate bleeding.

- Gastric Cancer or Erosive Gastritis: May have chronic, low-volume bleeding rather than acute hemorrhage.

Who Discovered Esophageal Varices?

Esophageal Varices themselves are not attributed to a specific individual. They were gradually recognized as a consequence of portal hypertension in patients with liver disease, a concept that evolved over centuries of clinical observation. 

The condition was first described in detail in the early 20th century, as the understanding of cirrhosis and portal hypertension advanced. 

The development of endoscopy in the mid-20th century allowed for more precise diagnosis and management of this life-threatening condition.

Key Considerations for EMS Providers

- Early Recognition: Suspect esophageal varices in any patient with massive hematemesis and a history of liver disease or alcohol abuse.

- Airway Safety: Suctioning and airway management are critical to prevent aspiration.

- Shock Management: Focus on maintaining perfusion with controlled fluid resuscitation.

- Definitive Treatment is Hospital-Based: EMS management is primarily supportive, with rapid transport to a facility that can perform endoscopy and possible surgical interventions.

Further Reading:

Alexander, M. & Belle, R. (2017) Advanced EMT: A Clinical Reasoning Approach (2nd Ed). Hoboken, New Jersey: Pearson Education

Brown, C. A. (2022) Walls Manual of Emergency Airway Management (5th Ed). Philadelphia, Pennsylvania: Lippincott, Williams & Wilkins

Bledsoe, B. E., Cherry, R. A. & Porter, R. S (2023) Paramedic Care: Principles and Practice (6th Ed) Boston, Massachusetts: Pearson

Meseeha, M., & Attia, M. (2023) Esophageal Varices. StatPearls. Treasure Island, Florida: StatPearls. Accessed September 28, 2024

Mistovich, J. J. & Karren, K. J. (2014) Prehospital Emergency Care (11th Ed). Hoboken, New Jersey: Pearson Education

Peate, I. & Sawyer, S (2024) Fundamentals of Applied Pathophysiology for Paramedics. Hoboken, New Jersey:  Wiley Blackwell

Thursday, June 06, 2024

EMS Pathophysiology - Anemia


Anemia is a condition marked by a reduction in the number of red blood cells (RBCs) or hemoglobin, impairing the blood’s ability to carry oxygen.
Recognizing and understanding the different types of anemia is crucial for EMS Providers, as this knowledge can guide appropriate prehospital care and improve patient outcomes.
Key Types of Anemia
* Iron Deficiency Anemia
  • Cause: Inadequate iron intake or absorption, blood loss.
  • Characteristics: Microcytic (small) and hypochromic (pale) RBCs.
  • Symptoms: Fatigue, weakness, pallor, shortness of breath
  • EMS Considerations: Assess for sources of bleeding (e.g., gastrointestinal), monitor vitals, consider oxygen therapy if indicated.
* Vitamin B12/Folate Deficiency Anemia
  • Cause: Insufficient dietary intake or absorption of Vitamin B12 or folate.
  • Characteristics: Macrocytic (large) and normochromic (normally colored) RBCs.
  • Symptoms: Fatigue, glossitis (inflamed tongue), neurological symptoms (e.g., numbness, tingling).
  • EMS Considerations: Assess neurological status, provide supportive care, monitor for signs of severe anemia.
* Hemolytic Anemia
  • Cause: Increased RBC destruction due to autoimmune disorders, infections, or genetic conditions like sickle cell disease.
  • Characteristics: Increased reticulocyte count (immature RBCs), jaundice.
  • Symptoms: Fatigue, jaundice, dark urine, pain (especially in sickle cell crises).
  • EMS Considerations: Pain management (especially for sickle cell crises), hydration, oxygen therapy, rapid transport for severe cases.
* Aplastic Anemia

  • Cause: Bone marrow failure leading to decreased production of RBCs, white blood cells (WBCs), and platelets.
  • Characteristics: Pancytopenia (reduced levels of all blood cells).
  • Symptoms: Fatigue, frequent infections, easy bruising, bleeding.
  • EMS Considerations: Monitor for signs of infection or bleeding, avoid invasive procedures when possible, supportive care, rapid transport.
* Anemia of Chronic Disease
  • Cause: Chronic infections, inflammatory diseases, malignancies.
  • Characteristics: Normocytic (normal size) and normochromic (normal color) RBCs, often with low iron availability.
  • Symptoms: Fatigue, weakness, symptoms related to the underlying chronic condition.
  • EMS Considerations: Assess and manage symptoms of the underlying condition, provide supportive care, monitor vitals.
General EMS Management of Anemia
  • Assessment: Conduct a thorough history and physical examination. Look for signs of pallor, jaundice, tachycardia, hypotension, and other symptoms indicative of anemia.
  • Oxygen Therapy: Administer oxygen as needed to improve tissue oxygenation. IV Access and Fluids: Establish IV access for potential fluid resuscitation, especially in cases of acute blood loss.
  • Monitor Vitals: Continuously monitor vital signs to detect any signs of deterioration.
  • Pain Management: Provide appropriate pain relief, particularly for patients with conditions like sickle cell disease.
  • Transport: Ensure rapid and safe transport to the appropriate medical facility for further evaluation and treatment.
Understanding the types and causes of anemia can help EMS Providers deliver better care and make informed decisions in the prehospital setting, ultimately improving patient outcomes.
Further Reading:
Alexander, M. & Belle, R. (2017) Advanced EMT: A Clinical Reasoning Approach (2nd Ed). Hoboken, New Jersey: Pearson Education
Bledsoe, B. E., Cherry, R. A. & Porter, R. S (2023) Paramedic Care: Principles and Practice (6th Ed) Boston, Massachusetts: Pearson
Mistovich, J. J. & Karren, K. J. (2014) Prehospital Emergency Care (11th Ed). Hoboken, New Jersey: Pearson Education

Peate, I. & Sawyer, S (2024) Fundamentals of Applied Pathophysiology for Paramedics. Hoboken, New Jersey:  Wiley Blackwell 

Saturday, April 13, 2024

EMS Neurological Emergencies - Seizure Disorder Pathophysiology


The pathophysiology of seizures involves complex changes in the electrical activity of the brain, leading to abnormal synchronization of neuronal firing and the generation of seizure activity. 

While the precise mechanisms underlying seizures can vary depending on the type of seizure and the underlying cause, there are several key components involved in the pathophysiology of seizures:

Neuronal Hyperexcitability: Seizures are characterized by abnormal, excessive, and synchronous neuronal activity in the brain. 

This hyperexcitability can arise from various factors, including changes in ion channel function, neurotransmitter imbalance, or alterations in neuronal connectivity.

Ion Channel Dysfunction: Ion channels play a crucial role in regulating the flow of ions (such as sodium, potassium, calcium, and chloride) across neuronal cell membranes, which is essential for maintaining normal neuronal excitability and function. 

Dysfunction of ion channels, either through genetic mutations or acquired alterations, can lead to abnormalities in neuronal excitability and contribute to seizure generation.

Imbalance of Excitatory & Inhibitory Neurotransmission: Normal brain function relies on a delicate balance between excitatory and inhibitory neurotransmission. 

Excitatory neurotransmitters, such as glutamate, promote neuronal activation, while inhibitory neurotransmitters, such as gamma-aminobutyric acid (GABA), dampen neuronal activity. 

Imbalances in the relative levels or function of these neurotransmitters can disrupt the normal inhibitory control of neuronal firing and contribute to seizure generation.

Aberrant Synchronization of Neuronal Firing: Seizures result from the abnormal synchronization of neuronal firing, leading to hypersynchronous activity within neuronal networks. This synchronized firing can spread rapidly throughout the brain, resulting in the characteristic clinical manifestations of seizures.

Network Dysfunction: Seizure activity often involves multiple brain regions and networks. 

Abnormalities in the connectivity and communication between different brain regions can facilitate the propagation of seizure activity and contribute to the generation of seizures.

Excitotoxicity & Neuroinflammation: Prolonged or recurrent seizure activity can lead to excitotoxicity, a process in which excessive release of excitatory neurotransmitters, such as glutamate, results in neuronal damage and cell death. 

Additionally, seizures can trigger neuroinflammatory processes, further exacerbating neuronal dysfunction and contributing to seizure generation.

Structural & Metabolic Factors: Structural abnormalities in the brain, such as tumors, vascular malformations, or cortical dysplasia, can disrupt normal neuronal circuitry and increase the likelihood of seizure activity. 

Metabolic disturbances, such as hypoglycemia, electrolyte imbalances, or mitochondrial disorders, can also trigger seizures by affecting neuronal function.

Overall, the pathophysiology of seizures involves a complex interplay of genetic, molecular, cellular, and network-level processes that lead to abnormal neuronal excitability and synchronization. 

Understanding these mechanisms is essential for developing targeted therapies aimed at preventing or controlling seizure activity.

Further Reading:

Bledsoe, B. E., Cherry, R. A. & Porter, R. S (2023) Paramedic Care: Principles and Practice (6th Ed) Boston, Massachusetts: Pearson

Huff, J.S. & Murr, N (2023) Seizure. Treasure Island, Florida: StatPearls Publishing https://www.ncbi.nlm.nih.gov/books/NBK430765/ Accessed April 24, 2024

Peate, I. & Sawyer, S (2024) Fundamentals of Applied Pathophysiology for Paramedics. Hoboken, New Jersey:  Wiley Blackwell