Acute Post hemorrhagic Anemia (Literature Review)
1. Dr. Samatbek Turdaliev
2. Kumar Shreemathy
Sudhakaran Shibaani Sre
(1. Teacher, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic
2. Students, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic.)
ABSTRACT
Acute post-hemorrhagic anaemia is a fast-onset disorder brought on by abrupt and substantial blood loss, which lowers the amount of red blood cells in circulation and impairs the transport of oxygen to tissues. Trauma, gastrointestinal bleeding, surgical bleeding, obstetric difficulties, and burst vascular lesions are common causes. The amount and pace of blood loss determine how severe anaemia is. Because both plasma and red cell loss happen at the same time, laboratory results may initially seem normal. However, within hours, hemodilution results in a discernible decrease in haemoglobin and haematocrit levels. Patients may exhibit clinical symptoms such as pallor, tachycardia, hypotension, disorientation, shortness of breath, and in extreme situations, shock symptoms. Clinical assessment, full blood counts, haemodynamic monitoring, and bleeding source identification are used to make the diagnosis. The goal of management is to stabilise patients quickly by oxygen therapy, blood transfusions, fluid resuscitation, and immediate haemorrhage control. Monitoring for problems and taking iron supplements are further treatments. To avoid organ dysfunction and enhance patient outcomes, early detection and timely intervention are crucial. Managing bleeding risk factors and promptly treating underlying illnesses are examples of preventive measures. Acute post-hemorrhagic anaemia is still a serious condition that needs to be treated with coordination.
Keywords: Acute post-hemorrhagic anemia, Blood loss, Hemodynamic instability, Transfusion therapy
INTRODUCTION
The quick loss of a significant amount of blood causes acute post-hemorrhagic anaemia, a serious clinical condition that causes the oxygen-carrying capacity of circulating red blood cells to rapidly diminish. It can occur in a variety of medical, surgical, and traumatic contexts and is one of the most frequent and potentially fatal effects of severe bleeding. Both the overall volume of blood loss and the rate of haemorrhage determine the severity of anaemia. Rapid blood loss causes circulatory instability and poor tissue perfusion because the body cannot effectively compensate. This could lead to shock, multiple organ failure, and even death if left untreated.
Acute bleeding can have a variety of underlying causes. Traumatic injuries, intraoperative or postoperative bleeding, gastrointestinal bleeding, obstetric problems, vascular ruptures, and bleeding disorders are among them. Because plasma and red blood cells are first lost at the same time, the degree of anaemia may not be readily apparent in early laboratory findings. However, fluid changes cause hemodilution within a few hours, which shows a significant drop in haematocrit and haemoglobin levels. Clinically, patients may exhibit indications of reduced organ perfusion, pallor, weakness, tachycardia, cold extremities, and hypotension.
In order to avoid serious problems, prompt diagnosis and action are essential. The main objectives of management are to locate the source of the bleeding, restore the volume of blood in circulation, and guarantee sufficient oxygen delivery. Fluid resuscitation, blood transfusions, oxygen therapy, and quick medical, endoscopic, or surgical haemorrhage control are all part of the treatment. Additionally, crucial to recovery are supportive treatments like iron supplementation and coagulopathy monitoring. Improving outcomes for patients with acute post-hemorrhagic anaemia requires an understanding of the pathogenesis, clinical presentation, and therapeutic strategies.
EPIDEMIOLOGY
In emergency, surgical, obstetric, and trauma care settings, acute post-hemorrhagic anaemia is a prevalent and clinically significant disease. The incidence of underlying causes such trauma, gastrointestinal bleeding, and maternal difficulties, as well as community factors and access to healthcare facilities, all have a significant impact on its epidemiology. Acute post-hemorrhagic anaemia is largely caused by trauma-related bleeding, which continues to be one of the major preventable causes of death worldwide, particularly among young adults. Inadequate access to prompt medical assistance raises acute blood loss-related morbidity and mortality in low- and middle-income nations.
One of the main causes in adults, especially in older populations, is gastrointestinal bleeding, which includes peptic ulcers, variceal haemorrhage, and cancers. Maternal morbidity and mortality are significantly increased by obstetric haemorrhage, particularly in areas with inadequate emergency obstetric treatment. Acute post-hemorrhagic anaemia is a significant concern in perioperative medicine since postoperative bleeding also makes up a significant percentage of cases. Acute haemorrhage causes millions of ER visits and hospital admissions each year, while the precise worldwide prevalence is hard to pinpoint due to inconsistent reporting. Reducing avoidable fatalities requires early detection, prompt intervention, and suitable care. In order to reduce the burden of acute post-hemorrhagic anaemia, healthcare planning, resource allocation, and preventative measures are guided by an understanding of epidemiological trends.
ETIOLOGY
Acute post-hemorrhagic anaemia is caused by an abrupt and substantial loss of blood, which quickly reduces the ability of circulating red blood cells to transfer oxygen, resulting in tissue hypoxia and haemodynamic instability. There are many different causes, including traumatic, surgical, gastrointestinal, obstetric, haematologic, and vascular.
1. Traumatic causes: Globally, trauma is a major cause of acute blood loss anaemia. Massive bleeding can be caused by blunt force trauma, industrial injuries, falls, piercing wounds, and traffic accidents. Young individuals are especially vulnerable to trauma-related bleeding, which frequently happens in prehospital or emergency situations where quick resuscitation is essential.
2. Surgical and Procedural Bleeding: One important iatrogenic cause is postoperative bleeding. Rapid blood loss can result from complications during or following surgeries, such as cardiac, gastrointestinal, orthopaedic, or vascular procedures. In individuals who are vulnerable, invasive diagnostic or therapeutic procedures like catheterizations, endoscopic procedures, or biopsies may also cause bleeding.
3. Gastrointestinal Bleeding: Acute anaemia in adults is frequently caused by gastrointestinal bleeding. Sudden, potentially fatal blood loss can result from conditions such severe haemorrhoids, diverticulosis, malignancies, esophageal varices (which are frequently caused by liver disease), and peptic ulcers. Susceptibility is increased by concomitant hepatic disease and anticoagulant medication.
4. Obstetric Causes: Particularly in environments with limited resources, obstetric haemorrhage continues to be a significant cause of maternal morbidity and mortality. If left untreated, postpartum haemorrhage, placental abruption, uterine rupture, retained placenta, and ectopic pregnancy can all result in fast anaemia.
5. Haematologic and Coagulation Disorders: Even with mild injuries or surgical treatments, patients with haemophilia, von Willebrand disease, thrombocytopenia, or those receiving anticoagulant or antiplatelet therapy are more likely to experience serious bleeding.
6. Vascular and Other Causes: Acute anaemia can also be brought on by ruptured aneurysms, arteriovenous malformations, severe epistaxis, and spontaneous intramuscular or retroperitoneal haemorrhage.
PATHOPHYSIOLOGY
Acute post-hemorrhagic anaemia occurs when the body's compensatory mechanisms are overwhelmed by quick and substantial blood loss, resulting in reduced oxygen delivery to tissues and organs. Haemodynamic alterations, cellular reactions, and time-dependent compensatory mechanisms are all part of the pathophysiology.
1. Immediate Effects of Blood Loss: The initial haemoglobin and haematocrit values may not adequately reflect the severity of anaemia since both red blood cells (RBCs) and plasma are lost proportionately in the first few minutes after haemorrhage. Reduced circulating blood volume is the main effect at this point, which lowers venous return, cardiac output, and arterial blood pressure.
2. Compensatory Mechanism: Cardiovascular Compensation: To sustain perfusion to essential organs like the heart, brain, and kidneys, tachycardia, increased myocardial contractility, and peripheral vasoconstriction take place. Redistribution of Blood Flow: To maintain perfusion to vital organs, blood is diverted from non-essential organs (skin, gastrointestinal system, and skeletal muscles). Neurohormonal Response: Blood pressure and fluid balance are maintained by the sympathetic nervous system's activation and the release of catecholamines, antidiuretic hormone (ADH), and the renin-angiotensin-aldosterone system (RAAS).
3. Delayed Hemodilution: The remaining red blood cells are diluted and the drop-in haemoglobin and haematocrit is shown when interstitial fluid moves into the intravascular compartment within a few hours. This results in the typical test results of anaemia.
4. Cellular and Tissue Effects: Anaerobic metabolism, lactic acid buildup, and tissue hypoxia are all brought on by reduced oxygen delivery. Organ dysfunction, which mostly affects the kidneys, liver, and central nervous system, develops if blood loss continues.
5. Secondary Complications: If prolonged or severe bleeding is not immediately stopped with fluid resuscitation, transfusions, and bleeding source control, it may result in coagulopathy, disseminated intravascular coagulation (DIC), and multi-organ failure.
STAGES OF BLOOD LOSS AND CLINICAL MANIFESTATIONS
Depending on the amount and rate of blood loss, acute post-hemorrhagic anaemia develops in stages, each of which is linked to distinct physiological reactions and clinical manifestations. For prompt detection and intervention, it is crucial to comprehend these phases.
1. Class I (Mild Blood Loss: <15% of Blood Volume)
Pathophysiology: Compensatory mechanisms maintain adequate tissue perfusion. Minimal hemodynamic changes occur.
Clinical Manifestations: Usually asymptomatic or may present with mild pallor and slight tachycardia. Blood pressure and urine output remain normal.
2. Class II (Moderate Blood Loss: 15–30% of Blood Volume)
Pathophysiology: Activation of sympathetic nervous system leads to increased heart rate and peripheral vasoconstriction.
Clinical Manifestations: Tachycardia, mild hypotension, anxiety, dizziness, pallor, delayed capillary refill, and reduced urine output may appear. Hemoglobin may remain near normal initially due to proportional plasma loss.
3. Class III (Severe Blood Loss: 30–40% of Blood Volume)
Pathophysiology: Compensatory mechanisms begin to fail; cardiac output decreases, and tissue hypoperfusion develops.
Clinical Manifestations: Marked tachycardia, hypotension, cold and clammy skin, confusion, agitation, oliguria, and severe pallor. Patients are at risk of shock.
4. Class IV (Life-Threatening Blood Loss: >40% of Blood Volume)
Pathophysiology: Compensatory mechanisms collapse; profound tissue hypoxia leads to multi-organ failure.
Clinical Manifestations: Severe hypotension, tachycardia or bradycardia (late), altered mental status or unconsciousness, anuria, metabolic acidosis, and signs of shock. Immediate resuscitation is required to prevent death.
The amount and rate of blood loss, the patient's initial health, and their ability to compensate all play a major role in how acute post-hemorrhagic anaemia manifests clinically. Due to a decreased oxygen-carrying capacity, patients may initially experience widespread exhaustion, weakness, and dyspnoea. Cerebral hypoperfusion can cause dizziness, lightheadedness, or even syncope, especially when standing. Cardiovascular symptoms are frequently noticeable; hypotension arises when blood loss overwhelms compensatory systems, while tachycardia first appears to sustain cardiac output.
Particularly in people who already have cardiac disease, weak, thready pulses, chest pain, or angina may manifest. Reduced tissue perfusion is indicated by peripheral symptoms such pallor of the lips, conjunctiva, and nail beds; chilly, clammy skin; and delayed capillary refill. Cerebral hypoxia is indicated by neurological abnormalities such as anxiety, restlessness, disorientation, and in extreme situations, lethargy or coma. While gastrointestinal hypoperfusion can result in nausea, vomiting, or discomfort in the abdomen, renal hypoperfusion can produce oliguria or anuria. Hours after the bleeding, laboratory results usually show decreasing haemoglobin and haematocrit levels, as well as metabolic acidosis and increased lactate in severe cases. The combination and intensity of these characteristics offer vital direction for immediate clinical evaluation and treatment.
DIAGNOSTIC EVALUATION
1.Clinical assessment
The first step in evaluating a patient with acute post-hemorrhagic anaemia is a comprehensive clinical assessment, which is essential for quickly determining the extent of blood loss and directing prompt treatment. Heart rate, blood pressure, respiration rate, and oxygen saturation are among the vital signs that clinicians pay particular attention to because they show tissue perfusion and haemodynamic stability. A physical examination looks for symptoms of shock, such as cold extremities and delayed capillary refill, as well as pallor and clammy skin. Additionally, neurological health, awareness, and mental orientation are evaluated because cerebral hypoperfusion may be indicated by confusion or lethargy.
2.Laboratory investigations
Anaemia can be objectively confirmed and quantified using laboratory tests. Haemoglobin and haematocrit levels are revealed by a complete blood count (CBC), and successive measures aid in monitoring trends while compensatory hemodilution takes place. A coagulation profile, which includes PT, aPTT, and platelet count, detects underlying bleeding issues or coagulopathy, whereas a reticulocyte count assesses bone marrow response. Serum electrolytes, renal function, liver function, and arterial blood gases, particularly lactate levels, are further assays that help evaluate the systemic effects of hypoperfusion and direct resuscitation techniques.
3.Imaging
When bleeding is not clinically evident, imaging techniques are used to identify the cause. While computed tomography (CT) can detect intra-abdominal or retroperitoneal bleeding, ultrasound is frequently utilised for quick bedside examination, especially in cases of trauma or postpartum haemorrhage. Angiography can be used therapeutically and diagnostically to identify and manage vascular sources of bleeding, while endoscopy is recommended for gastrointestinal bleeding. An integrated strategy for precise diagnosis, risk assessment, and prompt intervention in acute post-hemorrhagic anaemia is made up of clinical evaluation, laboratory testing, and imaging.
DIFFERENTIAL DIAGNOSIS
It's important to distinguish acute post-hemorrhagic anaemia from other rapid-onset anaemia causes or disorders that exhibit comparable clinical symptoms such exhaustion, pallor, tachycardia, and hypotension. Both immune-mediated and non-immune haemolytic anaemia can resemble acute anaemia, but instead of a history of acute blood loss, it is characterised by raised lactate dehydrogenase, increased reticulocyte counts, indirect hyperbilirubinemia, and occasionally haemoglobinuria. Instead of a sharp decline in haemoglobin, aplastic anaemia and bone marrow failure syndromes usually manifest as pancytopenia with a slow onset.
In contrast to the sudden haemodynamic compromise observed in acute haemorrhage, chronic blood loss anaemia, such as that caused by gastrointestinal cancer, heavy menstruation, or occult bleeding, typically develops gradually and permits compensatory mechanisms to stabilise the patient. Other illnesses, such extreme dehydration or plasma volume contraction, can initially conceal anaemia by artificially raising haemoglobin levels. Although they need to be confirmed in a lab, coagulopathies such as thrombocytopenia or disseminated intravascular coagulation (DIC) can cause bleeding. To determine the source of bleeding and rule out other causes of anaemia, accurate distinction depends on a thorough clinical history, physical examination, laboratory testing, and imaging. In order to guide effective care and reduce morbidity and mortality, it is imperative to promptly identify the true aetiology.
MANAGEMENT AND TREATMENT APPROACHES
1. Emergency Stabilization
Secure airway and ensure adequate oxygenation.
Continuous monitoring of vital signs: heart rate, blood pressure, respiratory rate, and oxygen saturation.
Establish large-bore intravenous access for rapid fluid and blood administration.
2. Fluid Resuscitation
Administer isotonic crystalloids (e.g., normal saline or Ringer’s lactate) to restore intravascular volume.
Maintain tissue perfusion and stabilize hemodynamics while preparing for transfusion.
3. Blood Transfusion
Transfuse packed red blood cells for moderate to severe anemia or ongoing hemorrhage.
Use additional blood components, such as fresh frozen plasma, platelets, or cryoprecipitate, in cases of massive hemorrhage or coagulopathy.
Monitor hemoglobin levels, hemodynamic status, and oxygen delivery during transfusion.
4. Control of Bleeding Source
Identify the source of hemorrhage promptly.
Use surgical intervention, endoscopic therapy, interventional radiology (e.g., embolization), or obstetric measures depending on etiology.
Adjunctive therapies may include iron supplementation, folic acid, and ongoing monitoring for complications.
SUPPORTIVE AND ADJUNCTIVE THERAPY
In addition to immediate stabilisation, fluid resuscitation, blood transfusion, and final control of the bleeding source, supportive and adjuvant therapy is a crucial part of the management of acute post-hemorrhagic anaemia. These actions are intended to maximise healing, avoid problems, and improve the patient's body's ability to withstand anaemia. Close clinical monitoring is essential; constant evaluation of peripheral perfusion, urine output, vital signs, and mental state gives important information regarding the patient's haemodynamic stability and directs continued therapies. In order to reduce tissue hypoxia and prevent organ failure, oxygen treatment is commonly used to increase tissue oxygenation, particularly in patients with severe anaemia or pre-existing cardiovascular or pulmonary problems.
Another important factor is nutritional support. While iron supplementation, either orally or intravenously, restores iron stores lost during haemorrhage and promotes red blood cell synthesis, folic acid and vitamin B12 administration improves erythropoiesis. Adjunctive transfusion of blood components, such as fresh frozen plasma, platelets, or cryoprecipitate, corrects clotting deficits and aids in haemostasis in patients with coagulopathy or persistent bleeding. Other supporting methods that enhance patient comfort and recuperation include pain treatment, infection avoidance, and electrolyte and fluid balance maintenance.
Additionally, by reducing consequences like organ failure, metabolic problems, or recurrent bleeding, these treatments are crucial to long-term results. Comprehensive care is ensured by close monitoring, laboratory testing, and modifying supportive measures in response to the patient's changing clinical status. Supportive and adjuvant therapy essentially improves prognosis and lowers morbidity and mortality in patients with acute post-hemorrhagic anaemia by providing the physiological and metabolic support required for recovery while allowing definitive treatments to take effect.
COMPLICATION
Many consequences can result from acute post-hemorrhagic anaemia, especially if blood loss is significant, fast, or poorly controlled. Hypovolemic shock, which is caused by insufficient blood volume in circulation and consequent tissue hypoperfusion, is the most serious and immediate consequence. Shock can develop into multi-organ dysfunction that affects the kidneys, liver, heart, and brain if it continues. Prolonged hypotension can cause renal problems such acute tubular necrosis, and hepatic ischaemia might affect coagulation and metabolic processes. Patients with pre-existing cardiac illness are more prone to experience cardiovascular problems, such as myocardial ischaemia, arrhythmias, or heart failure. Confusion, sluggishness, or possibly irreparable neurological impairment are symptoms of cerebral hypoxia.
Other complications include coagulopathy, either as a primary contributor to ongoing hemorrhage or secondary to massive transfusion, and metabolic disturbances, including acidosis and electrolyte imbalances. Recurrent or uncontrolled bleeding can exacerbate anemia and further compromise organ perfusion. In the long term, patients may experience fatigue, reduced exercise tolerance, and impaired quality of life, particularly if iron stores remain depleted or if there is inadequate recovery of hemoglobin levels.
PROGNOSIS
The amount and pace of blood loss, the promptness of medical care, the patient's age, and comorbidities all have a significant impact on the prognosis of acute post-hemorrhagic anaemia. Survival rates are greatly increased and complications are decreased with early detection, quick resuscitation, and complete control of the bleeding source. Most individuals can make a full recovery with prompt and proper care. However, excessive bleeding or delayed action is linked to high morbidity and mortality, highlighting the significance of prompt identification, ongoing observation, and all-encompassing care.
CONCLUSION
Abrupt and severe blood loss can cause acute post-hemorrhagic anaemia, a potentially fatal illness that can cause tissue hypoxia, decreased oxygen carrying capacity, and organ failure. Early detection and treatment are crucial because of its many causes, which include trauma, surgical difficulties, gastrointestinal bleeding, obstetric haemorrhage, and coagulation abnormalities. While laboratory testing and imaging help confirm anaemia and identify the source of bleeding, clinical detection depends on a thorough evaluation of vital signs, physical examination, and symptoms such pallor, tachycardia, hypotension, and disturbed mental status. Emergency stabilisation, fluid resuscitation, blood transfusions, controlling the cause of bleeding, and supportive and adjuvant therapy like iron, folic acid, oxygen supplements, and coagulopathy correction are all part of the complex management. While delayed or insufficient therapy can result in consequences like shock, multi-organ failure, and death, prompt intervention dramatically lowers morbidity and mortality. Optimising results requires interdisciplinary care, early detection, and preventive measures. In order to improve patient prognosis and survival, healthcare personnel must have a thorough understanding of the pathogenesis, clinical symptoms, and evidence-based management of acute post-hemorrhagic anaemia.
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