Causes and mechanisms of vascular wall damage
Loss of vascular bed integrity can occur through several completely different scenarios:
- Mechanical trauma (haemorrhagia per rhexin). Occurs from direct physical impact: open wounds, closed ruptures from impacts, as well as thermal injuries (burns or frostbite).
- Arrosive processes (haemorrhagia per diabrosin). The vessel wall is destroyed not from the outside, but due to an ongoing pathological process. This may be the ingrowth and breakdown of a malignant tumor, deep necrosis, or purulent tissue melting.
- Diapedesis (haemorrhagia per diapedesin). A specific mechanism in which blood transudes through the walls of the smallest vessels (capillaries, venules) without their visible anatomical damage. The cause lies in molecular changes in permeability. It occurs in vitamin C deficiency, uremia, severe infections (smallpox, scarlet fever), phosphorus intoxication, and hemorrhagic vasculitis.
Hemostasis disorders
The severity of blood loss does not always correlate with the size of the damaged vessel. In coagulopathies, even microtrauma can lead to massive blood effusion. Such disorders are divided into several groups:
- Hereditary pathologies. Include hemophilia (deficiency of plasma factors VIII or IX) and Werlhof's disease, in which the platelet count is critically reduced.
- Acquired (DIC syndrome). Disseminated intravascular coagulation syndrome develops in shock, sepsis, or crush syndrome. Due to multiple thrombus formation, clotting factors are depleted, a hypocoagulation phase sets on, and spontaneous hemorrhages occur.
- Iatrogenic (drug-induced). Caused by taking anticoagulants (disrupting factor synthesis or directly affecting thrombus formation, like heparin), fibrinolytics, and NSAIDs (reducing platelet aggregation).
- Cholemic. Occur in patients with jaundice. Due to hepatic failure, vitamin K absorption is impaired, leading to a drop in clotting factor levels. It is corrected by plasma transfusion, vitamin K administration, and cryoprecipitate.
Classification by the type of bleeding vessel
The nature of blood outflow directly depends on the caliber and type of the damaged trunk:
- Arterial. The blood has a bright scarlet hue and spurts out in a pulsating jet. The larger the artery, the faster critical blood loss ensues.
- Venous. Dark blood flows out evenly and continuously. However, if a large artery runs nearby, transmitted pulsation is possible. Wounds to the cervical or subclavian veins are extremely dangerous: inspiration creates negative pressure in them, which can lead to air aspiration (air embolism).
- Capillary. Mixed blood oozes across the entire surface of the wound. If wiped away, it immediately reappears.
- Parenchymal. Occurs when internal organs are damaged (liver, kidneys, spleen). Anatomically, the vessels there do not collapse, making such bleeding extremely massive and very difficult to stop.
Internal hemorrhages and their consequences
If blood does not escape to the exterior, it may accumulate in the body's tissues or cavities.
When tissues are soaked, a hemorrhage (imbibition) forms. If there is a lot of blood and it dissects tissues, a hematoma—an artificial cavity—is formed. A hematoma may resolve, become suppurated, calcify (petrification), or turn into a cyst, becoming covered with a connective tissue capsule.
Hemorrhages into serous cavities (abdominal, pleural) differ in that they almost never stop on their own. Two factors hinder this: the suction effect due to negative pressure and blood defibrination (fibrin precipitates on the serous membranes, depriving the blood of its ability to form a thrombus).
Of particular danger are occult hemorrhages (e.g., from gastrointestinal ulcers). They proceed without external symptoms, lead to severe anemia, and are detected only by special methods (e.g., the Gregersen test for occult blood in feces).
Briefly: answers to topical questions
What types of internal hemorrhages exist depending on the anatomical cavity where the blood escapes?
Depending on the anatomical cavity into which the blood escapes, the following types of internal hemorrhages are distinguished:
- Hemopericardium is the accumulation of blood in the pericardial cavity.
- Hemothorax is the accumulation of blood in the pleural cavity.
- Hemoperitoneum is the accumulation of blood in the abdominal cavity.
- Hemarthrosis is the accumulation of blood in a joint cavity.
How are hemorrhages classified according to the time of their occurrence?
According to the time of occurrence, hemorrhages are classified into primary and secondary.
- Primary — occur immediately at the time of injury (vascular damage).
- Secondary — develop some time after the injury and the arrest of the initial hemorrhage.
Secondary hemorrhages are additionally subdivided into:
- Early — occur within the first 3 days.
- Late — occur after a significant period of time (from 3 days to several weeks).
What methods exist for the temporary arrest of external arterial bleeding?
The following methods are used for emergency temporary arrest of external arterial bleeding:
- Digital compression of an artery — compression of the arterial trunk against underlying bony prominences proximal to the injury site.
- Tourniquet application — the most reliable method, used mainly on limbs.
- Application of a pressure bandage — used for small arteries.
- Wound tamponade — tight packing of a gauze swab secured with a pressure bandage.
- Flexion of the extremity at the joint — fixation of the extremity in the position of maximum flexion.
What are the main groups of methods for definitive hemostasis?
Methods for definitive hemostasis are classified into four main groups:
- Mechanical
- Physical
- Chemical and biological
- Combined
Mechanical methods include applying a clamp to the vessel and its ligation. The most reliable method is vessel ligation within the wound: isolating the central and peripheral ends of the vessel, grasping them with hemostatic clamps, and ligating them.
What clinical and laboratory parameters determine the severity of acute blood loss?
The severity of acute blood loss is determined by a number of clinical and laboratory parameters reflecting the volume of lost blood and the reduction in circulating blood volume (CBV).
Clinical parameters:
- Skin integument — color (pallor, cyanosis, acrocyanosis), temperature, presence of cold sweat.
- Pulse — rate (tachycardia), volume, and tension.
- Blood pressure (BP) — level of decrease (hypotension).
- Peripheral circulation — state of the capillary bed.
- Diuresis — hourly monitoring of urine output.
- Shock index (Allgower index).
Laboratory and instrumental parameters:
- Hemoglobin and hematocrit — decrease in their concentration.
- BVL — determination of blood volume level.
- CVP — measurement of central venous pressure.
To remember the outcomes of a hematoma, use the acronym RSNI: Resolution, Systad [Cyst], Necrosis [Suppuration], Induration [Calcification].
What else to study on this topic
- Pathogenesis and stages of DIC syndrome
- Mechanisms of cholemic bleeding in liver failure
- Laboratory diagnostic methods for occult bleeding (Gregersen test)
- Types of iatrogenic bleeding: effect of heparin and NSAIDs on hemostasis
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