Vitamin K Deficiency

Vitamin K deficiency is a serious nutritional disorder affecting the blood clotting system of farm animals, leading to impaired coagulation and potentially life-threatening hemorrhage. This fat-soluble vitamin is essential for the synthesis of several clotting factors in the liver, and without adequate vitamin K, animals cannot produce functional coagulation proteins. The condition can arise from primary dietary insufficiency, destruction of vitamin K by antagonistic compounds, or interference with vitamin K metabolism. While relatively uncommon in most livestock species due to bacterial synthesis in the gastrointestinal tract, certain circumstances create significant risk for vitamin K deficiency and its severe consequences.

The manifestation of vitamin K deficiency varies considerably across farm animal species based on their ability to synthesize vitamin K through gut bacteria and their dietary sources of this nutrient. Poultry are the species most commonly affected by dietary vitamin K deficiency because birds have a relatively short digestive tract that limits bacterial vitamin K synthesis and absorption. Ruminants rarely develop primary vitamin K deficiency due to extensive bacterial production in the rumen, but they are susceptible to functional deficiency when fed moldy sweet clover containing dicoumarol, a potent vitamin K antagonist. Pigs and horses fall between these extremes, with moderate susceptibility to deficiency under certain circumstances.

The economic and welfare impact of vitamin K deficiency can be severe when it occurs. Affected animals may experience spontaneous hemorrhage, prolonged bleeding from minor wounds, and internal bleeding that can be rapidly fatal. In poultry operations, outbreaks of hemorrhagic disease can cause significant mortality before the underlying cause is identified. Sweet clover poisoning in cattle has historically caused substantial losses, particularly in operations using improperly cured hay or silage from sweet clover fields. The insidious nature of anticoagulant effects means that clinical signs may not appear until clotting factor reserves are severely depleted, often several days after exposure begins.

Effective management of vitamin K deficiency requires understanding the various routes by which deficiency can develop and implementing appropriate prevention and treatment strategies. Recognition of risk factors specific to each species and production system allows targeted intervention before clinical disease occurs. When hemorrhagic signs appear, prompt diagnosis and vitamin K administration can be life-saving if intervention occurs before blood loss becomes critical. Prevention through adequate dietary supplementation in susceptible species and avoidance of vitamin K antagonists remains the most effective approach to this potentially devastating condition.

The primary cause of true dietary vitamin K deficiency is inadequate intake in species that cannot synthesize sufficient quantities through bacterial fermentation in the gastrointestinal tract. Poultry represent the most susceptible species because their short digestive tract and rapid transit time limit the opportunity for bacterial vitamin K synthesis and absorption. Young chicks are particularly vulnerable because their immature gut flora has not yet established robust vitamin K production. Feeds that have been heat-processed or stored for extended periods may have reduced vitamin K content. Diets based primarily on grains without adequate green plant material or supplementation may not provide sufficient vitamin K for poultry, especially during periods of rapid growth or egg production.

Sweet clover poisoning represents the most significant cause of functional vitamin K deficiency in ruminants and creates a syndrome indistinguishable from primary deficiency. When sweet clover hay or silage becomes moldy, the coumarin naturally present in the plant is converted to dicoumarol by fungal action. Dicoumarol is a potent antagonist of vitamin K that blocks the enzyme responsible for recycling vitamin K after it participates in clotting factor synthesis. The result is a functional deficiency of vitamin K even when dietary intake is adequate. The condition develops insidiously as clotting factor reserves become depleted over days to weeks of consuming contaminated feed, with clinical signs often appearing suddenly when coagulation capacity falls below critical thresholds.

Environmental and management factors significantly influence the risk of vitamin K deficiency in livestock populations. In poultry, antibiotic treatment that eliminates gut bacteria can reduce endogenous vitamin K synthesis, making dietary supplementation more critical. Sulfonamide drugs are particularly associated with this effect. Intestinal diseases that impair fat absorption reduce vitamin K uptake since it is a fat-soluble vitamin. Liver disease can impair the synthesis of clotting factors even when vitamin K status is adequate. In cattle, improper curing or storage of sweet clover hay creates the conditions for dicoumarol formation. Feeding spoiled or moldy feeds of any type poses potential risk, as various mycotoxins can interfere with vitamin K metabolism.

Risk factors for developing clinical disease include species, age, physiological state, and concurrent health conditions. Young animals of all species have limited reserves of clotting factors and can develop clinical signs more rapidly than adults. Animals with liver disease may have impaired clotting factor synthesis regardless of vitamin K status. Concurrent disease or stress increases metabolic demands and may deplete reserves more rapidly. Trauma or surgical procedures that cause bleeding reveal subclinical coagulation deficits that might otherwise remain undetected. Pregnant animals face particular risk because hemorrhage during parturition can be catastrophic when coagulation is impaired.

The pathophysiology of vitamin K deficiency involves failure to synthesize functional clotting factors required for normal hemostasis. Vitamin K serves as an essential cofactor for an enzyme that activates several clotting factors, including factors II, VII, IX, and X, by adding a chemical group necessary for their function. Without adequate vitamin K or when vitamin K recycling is blocked by antagonists, the liver produces these clotting factors in an inactive form. As existing functional clotting factors are depleted through normal turnover, the animal's ability to form blood clots progressively deteriorates. Factor VII, with the shortest half-life, becomes depleted first, followed by the other factors over subsequent days. Once clotting factor activity falls below approximately 20 to 30 percent of normal, spontaneous hemorrhage becomes likely.

Early warning signs of vitamin K deficiency are typically subtle and may not be recognized until significant coagulation impairment has developed. Animals in the early stages of deficiency may show no obvious abnormalities because the bleeding tendency only becomes apparent when the coagulation system is challenged. The first indication of a problem may be prolonged bleeding from routine procedures such as blood collection, ear tagging, or dehorning. Minor wounds that would normally stop bleeding quickly continue to ooze blood. Careful observation may reveal small hemorrhages in the skin, mucous membranes, or visible portions of the sclera. These subtle signs often go unnoticed until more severe hemorrhage occurs.

As vitamin K deficiency progresses, bleeding manifestations become more obvious and affect multiple body systems. Subcutaneous hemorrhages appear as soft, fluctuant swellings that may develop spontaneously or following minor trauma. Hematomas can form in muscle tissue, causing lameness and pain. Bleeding into joints produces sudden lameness with joint swelling and heat. Epistaxis, or nosebleeds, may occur spontaneously. Bloody urine or feces indicates hemorrhage into the urinary or gastrointestinal tracts. In laying hens, blood spots in eggs and hemorrhage into developing follicles may occur. Affected animals often develop progressive weakness and pallor as blood loss continues.

Behavioral changes in animals with vitamin K deficiency reflect the effects of blood loss and the discomfort associated with hemorrhage. Affected animals become weak and lethargic as anemia develops from continued bleeding. They may be reluctant to move due to painful hematomas or joint hemorrhages. Decreased feed intake accompanies general malaise, further weakening compromised animals. Animals may be found lying down more frequently and may resist efforts to move them. In severe cases, affected animals become progressively more obtunded as shock develops from acute blood loss.

Physical examination findings reflect the hemorrhagic nature of this condition. Pale mucous membranes indicate anemia from blood loss, with the degree of pallor correlating with the severity and duration of hemorrhage. Heart rate is typically elevated as the cardiovascular system attempts to compensate for reduced blood volume. Respiratory rate may be increased as tissues become oxygen-deprived from anemia. Palpation may reveal fluctuant subcutaneous swellings representing hemorrhage beneath the skin. Joint effusion may be present in cases with hemarthrosis. Petechiae, or pinpoint hemorrhages, may be visible on mucous membranes and non-pigmented skin.

Symptom progression follows a predictable pattern as coagulation ability continues to decline. Early, mild bleeding gives way to more significant hemorrhage as clotting factors become further depleted. Internal hemorrhage may occur without external evidence, causing rapid deterioration from blood loss into body cavities. Hemorrhage into the brain or spinal cord can cause sudden neurological signs including seizures, paralysis, or death. Bleeding into the chest cavity produces respiratory distress as the lungs become compressed. Abdominal hemorrhage causes progressive weakness and collapse as blood accumulates in the peritoneal cavity. Without intervention, affected animals often die from hypovolemic shock.

Emergency symptoms requiring immediate veterinary intervention include massive external hemorrhage, signs of internal bleeding such as sudden weakness and pale membranes without obvious external blood loss, respiratory distress from pleural hemorrhage, and neurological signs suggesting central nervous system bleeding. Any animal found dead with evidence of hemorrhage should prompt immediate investigation of remaining animals and feed sources. Multiple animals showing bleeding tendency simultaneously strongly suggests a herd-level problem requiring urgent action to prevent additional cases and deaths.

Clinical examination in suspected vitamin K deficiency focuses on identifying evidence of hemorrhage and assessing the severity of blood loss. Examination of mucous membranes for pallor and petechiae provides information about both anemia and active hemorrhage. Palpation of the body identifies subcutaneous hematomas, joint effusions, and other localized bleeding. Assessment of vital signs reveals the tachycardia and tachypnea associated with blood loss and anemia. Documentation of prolonged bleeding from any wounds or venipuncture sites directly demonstrates impaired coagulation. Complete history should include questions about feed sources, recent antibiotic use, and any known exposure to sweet clover or other potential vitamin K antagonists.

Diagnostic testing provides objective confirmation of coagulopathy and helps differentiate vitamin K deficiency from other causes of bleeding disorders. Prothrombin time and activated partial thromboplastin time are typically prolonged in vitamin K deficiency, reflecting the impaired synthesis of multiple clotting factors. Specific clotting factor assays can quantify the degree of deficiency for individual factors if available. Proteins induced by vitamin K absence or antagonism can be measured to confirm vitamin K-related coagulopathy. Complete blood count reveals the anemia resulting from hemorrhage and helps assess the severity of blood loss. Blood chemistry evaluation may identify concurrent liver disease affecting clotting factor synthesis.

Differential diagnosis for bleeding disorders in farm animals includes several conditions beyond vitamin K deficiency. Thrombocytopenia, or low platelet count, can produce bleeding that resembles vitamin K deficiency but involves a different component of hemostasis. Disseminated intravascular coagulation causes widespread hemorrhage through consumption of clotting factors and platelets. Inherited coagulation factor deficiencies exist in some species but are rare. Severe liver disease can impair clotting factor synthesis independent of vitamin K status. Rodenticide poisoning with anticoagulant compounds produces clinical and laboratory findings identical to sweet clover poisoning. Vascular disorders causing fragile blood vessels can produce petechiae and hemorrhage without coagulation abnormalities.

Herd-level diagnostics are essential when vitamin K deficiency is suspected because the underlying causes typically affect multiple animals. Careful review of feed sources identifies potential exposure to moldy sweet clover or other vitamin K antagonists. Feed analysis can detect dicoumarol in suspect hay or silage and quantify the level of contamination. Evaluation of medication records identifies recent antibiotic use that might affect gut flora and vitamin K synthesis. Sampling representative animals for coagulation testing helps characterize the scope of the problem in the population. Necropsy of animals that die provides definitive evidence of hemorrhagic disease and helps rule out other causes of death in the herd.

Emergency and immediate treatment of vitamin K deficiency focuses on halting hemorrhage, replacing lost blood volume, and restoring coagulation ability. Vitamin K1, also known as phytonadione, is the treatment of choice and should be administered as soon as vitamin K deficiency is suspected. Injectable formulations provide rapid delivery, though the full effect on clotting factor synthesis requires several hours to become apparent. The initial dose may be repeated at 12 to 24 hour intervals depending on severity and response. Fresh whole blood or plasma transfusion provides immediate coagulation factors and replaces lost blood volume in severely affected animals, buying time for vitamin K therapy to take effect. For food-producing animals, vitamin K products must be used according to label directions with attention to withdrawal times.

Medical management following initial stabilization continues vitamin K supplementation until normal coagulation is restored and maintained. Oral vitamin K1 supplementation can follow initial injectable treatment and may be continued for several weeks in cases involving prolonged exposure to vitamin K antagonists like dicoumarol. The duration of treatment depends on the cause of deficiency, with simple dietary deficiency requiring shorter treatment than antagonist-induced deficiency. Monitoring coagulation times helps guide the duration of therapy and confirms restoration of normal hemostasis. Supportive care including iron supplementation may help address anemia from blood loss, though the primary focus remains on preventing further hemorrhage.

Surgical intervention may be necessary to address complications of vitamin K deficiency rather than the deficiency itself. Large hematomas may require drainage to relieve pressure on surrounding structures and prevent infection. Hemorrhage into body cavities may necessitate surgical exploration to identify and control bleeding sources once coagulation has been restored. Joint lavage may benefit animals with significant hemarthrosis. Any surgical procedures must be delayed until adequate coagulation has been restored through vitamin K therapy, as surgery on animals with active coagulopathy carries extreme risk of uncontrollable hemorrhage.

Supportive care is critical for animals weakened by blood loss while awaiting response to vitamin K therapy. Strict rest minimizes trauma that could trigger additional hemorrhage. Soft bedding prevents pressure on hematomas and provides comfort. Easy access to feed and water without requiring extensive movement accommodates weakness. Protection from aggressive herdmates prevents trauma-induced bleeding. Monitoring for signs of continued hemorrhage or deterioration guides the intensity of intervention. Nursing care for recumbent animals prevents secondary complications including pressure sores and aspiration.

Herd treatment protocols address the population-level risk when vitamin K antagonist exposure has occurred. All animals that have consumed contaminated feed should receive vitamin K1 prophylactically, as clinical signs may not appear until coagulation is severely impaired. Immediate removal of the contaminated feed source prevents further exposure. Testing of remaining animals for prolonged coagulation times identifies those requiring treatment before clinical hemorrhage occurs. Treatment continues until sufficient time has elapsed for complete elimination of the antagonist and normalization of clotting factors. In poultry operations experiencing outbreaks, vitamin K supplementation of the entire flock through water or feed provides efficient mass treatment.

Treatment decisions must consider the severity of disease, likelihood of recovery, and economic factors. Animals with mild coagulopathy detected before significant hemorrhage generally respond well to vitamin K therapy. Those with severe anemia from blood loss require more intensive support and carry a more guarded prognosis. Animals with hemorrhage into critical structures including the brain or spinal cord rarely survive even with aggressive treatment. The cost of intensive care including blood transfusions may exceed the value of affected animals, though valuable breeding stock may warrant greater investment. Veterinary guidance helps determine appropriate treatment intensity based on individual circumstances.

The recovery timeline for vitamin K deficiency varies depending on the cause of deficiency and the severity of clinical disease. Animals with simple dietary deficiency respond rapidly to vitamin K supplementation, with improved coagulation tests often evident within 12 to 24 hours and normalization within a few days. Cases involving vitamin K antagonist exposure require longer treatment because the antagonist must be eliminated from the body before normal vitamin K cycling resumes. Dicoumarol has a long half-life in cattle, and treatment for sweet clover poisoning may be required for two to four weeks or longer. Recovery from blood loss anemia takes additional time, with red blood cell regeneration requiring several weeks for complete correction.

Post-treatment care and monitoring ensure complete recovery and prevent relapse. Serial coagulation testing confirms restoration of normal hemostasis and guides decisions about discontinuing vitamin K supplementation. Packed cell volume or hematocrit monitoring tracks recovery from anemia. Animals should be protected from trauma that could trigger hemorrhage during the recovery period, even after coagulation tests have normalized. Gradual return to normal activity minimizes the risk of rebleeding. For cases involving antagonist exposure, monitoring should continue for several days after discontinuing treatment to confirm that coagulopathy does not recur.

Prognosis depends primarily on the severity of hemorrhage before treatment and the structures affected by bleeding. Animals treated before significant blood loss occurs generally have an excellent prognosis for complete recovery. Those with moderate anemia typically recover fully with appropriate supportive care and time for red blood cell regeneration. Severe anemia from massive hemorrhage carries a more guarded prognosis, particularly if shock has developed. Hemorrhage into critical organs including brain, spinal cord, or lungs often results in permanent damage or death despite treatment. Animals that recover fully have no expected long-term consequences from the episode.

Return to production considerations focus on ensuring complete recovery before resuming normal activities. Animals should have documented normalization of coagulation tests before returning to situations where minor trauma is likely. Breeding animals should recover completely before entering the breeding herd, as parturition creates bleeding risk. Growing animals may experience temporary setbacks in growth performance but typically catch up once recovered. Documentation of treatment and withdrawal time compliance is essential for any animals destined for food production. Identification and elimination of the source of vitamin K antagonism prevents recurrence in affected herds.

Vaccination is not applicable to vitamin K deficiency, but preventive supplementation protocols effectively prevent dietary deficiency in susceptible species. Vitamin K3, also known as menadione, is commonly added to poultry feeds at levels designed to meet requirements even when gut synthesis is reduced. Special attention to vitamin K supplementation is warranted in young chicks, during antibiotic therapy, and during periods of intestinal disease that might impair synthesis or absorption. Commercial poultry feeds are typically adequately supplemented, but custom-mixed rations or feeds for organic production may require verification of adequate vitamin K content. Injectable vitamin K administered to day-old chicks provides immediate protection during the vulnerable neonatal period.

Biosecurity in the context of vitamin K deficiency focuses primarily on feed safety rather than disease transmission. Inspecting hay and silage for mold before feeding helps identify potentially contaminated sweet clover. Proper curing and storage of sweet clover hay reduces the risk of dicoumarol formation. Avoiding feeding sweet clover altogether eliminates the risk entirely, though this forfeits a potentially valuable forage crop. Ensuring that rodenticides and other anticoagulant compounds are stored securely and used only as directed prevents accidental livestock exposure. Screening feeds for mycotoxins may identify contamination before clinical problems develop.

Nutritional prevention in ruminants focuses on avoiding vitamin K antagonists rather than supplementation. Dietary vitamin K supplementation in ruminants is generally unnecessary due to robust rumen bacterial synthesis. The key preventive strategy is preventing consumption of moldy sweet clover. If sweet clover must be used, ensuring proper curing, limiting the proportion of the diet from this source, and diluting with other forages reduces risk. Feeding sweet clover hay or silage for no more than two to three weeks, followed by a similar period without it, prevents accumulation of dicoumarol to dangerous levels. Testing suspect sweet clover for dicoumarol content before feeding allows informed decisions about its safety.

Management practices that support normal vitamin K status complement supplementation and feed management. Maintaining healthy gut flora in monogastric species supports endogenous vitamin K synthesis. Judicious antibiotic use minimizes disruption of beneficial bacteria. Prompt treatment of intestinal disease reduces periods of impaired vitamin K absorption. Avoiding unnecessary stress supports normal digestive function. Proper storage of all feeds prevents mold growth and potential mycotoxin contamination. Routine observation of animals for early signs of bleeding problems allows intervention before severe hemorrhage occurs.

Quarantine and testing protocols for vitamin K status are generally not routinely practiced but may be warranted in specific circumstances. Testing of sweet clover hay or silage for dicoumarol content before feeding to cattle provides assurance of safety. Coagulation testing of animals that have consumed suspect feeds identifies subclinical coagulopathy before hemorrhage occurs. In poultry operations with historical problems or unique risk factors, periodic verification of vitamin K adequacy through either feed testing or coagulation screening may be valuable. Documentation of supplement inclusion in custom-mixed rations ensures that intended nutrition is actually delivered.

Daily management and monitoring for vitamin K deficiency prevention integrates awareness of bleeding risk into routine animal care. Observing animals during and after procedures that cause minor wounds allows early detection of prolonged bleeding. Monitoring for unexplained bruising, hematomas, or weakness that might indicate internal hemorrhage catches developing problems early. Ensuring that appropriate supplements are being delivered to susceptible species confirms that prevention programs are functioning as intended. Recording any observations of bleeding problems creates documentation for trend analysis and veterinary consultation if concerns arise.

Housing and environmental management for vitamin K deficiency prevention focuses on feed storage and minimizing trauma risk. Proper hay storage facilities that prevent moisture accumulation and mold growth protect against dicoumarol formation in sweet clover. Climate-controlled storage for vitamin supplements maintains their potency. Facility design that minimizes sharp edges and collision hazards reduces trauma that could reveal subclinical coagulopathy. Non-slip flooring prevents falls that might cause internal hemorrhage in marginally affected animals. Adequate space reduces aggression and associated injuries.

Herd health programs should incorporate consideration of vitamin K status, particularly in species or situations with elevated risk. Feed formulation review ensures adequate vitamin K supplementation for poultry and other susceptible animals. Monitoring of sweet clover usage in cattle operations prevents excessive exposure to potential dicoumarol sources. Veterinary involvement in investigating any unexplained bleeding episodes ensures appropriate diagnosis and prevention of recurrence. Integration of vitamin K considerations with overall nutritional monitoring provides comprehensive assessment of herd health status.

Record keeping and monitoring systems support prevention through documentation and trend analysis. Recording any episodes of prolonged bleeding or unexplained hemorrhage creates a database for pattern recognition. Documenting feed sources, supplement usage, and any changes to the feeding program facilitates investigation if problems occur. Tracking usage of sweet clover and other potentially problematic forages allows correlation with any health issues. Maintaining supplier information for feeds and supplements supports rapid investigation and notification if contamination is discovered.

Economic considerations in vitamin K deficiency prevention are generally favorable for appropriate intervention. The cost of vitamin K supplementation in poultry feeds is minimal and provides insurance against potentially devastating hemorrhagic disease outbreaks. Testing sweet clover for dicoumarol before feeding costs less than treating affected animals or the losses from sudden deaths. Proper feed storage to prevent mold growth protects the overall investment in feeds beyond just vitamin K considerations. The economic impact of a severe outbreak including mortality, treatment costs, and production losses far exceeds the modest cost of prevention programs. Investing in feed quality and appropriate supplementation represents sound economic management alongside good animal husbandry.

High-risk breeds and species for vitamin K deficiency are determined primarily by digestive tract anatomy and management factors rather than genetics. Poultry are the species most commonly affected by dietary vitamin K deficiency due to their limited capacity for gut bacterial synthesis. Among poultry, rapidly growing broilers and high-producing layers have the greatest requirements. Turkeys may be more susceptible than chickens to hemorrhagic syndromes related to vitamin K inadequacy. Ruminants rarely experience primary dietary deficiency but are uniquely susceptible to sweet clover poisoning, with cattle and sheep both affected. Monogastric species including pigs and horses occupy intermediate positions, with some capacity for gut synthesis but greater susceptibility than ruminants.

Production type influences vitamin K requirements and risk profiles. High-producing laying hens have elevated requirements to support eggshell and egg content production. Rapidly growing meat birds have increased metabolic demands. Breeding animals face particular risk from potential hemorrhage during parturition. Young animals of all species have limited reserves and may develop clinical signs more rapidly than adults. Animals receiving antibiotic therapy that disrupts gut flora have temporarily increased requirements. Cattle operations that utilize sweet clover as a forage crop face specific risk from potential dicoumarol exposure.

Genetic selection has not specifically addressed vitamin K metabolism in farm animal populations. Some variation in coagulation factor efficiency or vitamin K recycling enzymes may exist but has not been characterized for selection purposes. The focus for managing vitamin K deficiency risk remains on appropriate nutrition and avoidance of antagonists rather than genetic approaches. Producers should ensure that nutrition programs meet the requirements of their production genetics rather than expecting animals to adapt to inadequate vitamin K supply. Documentation of any bleeding tendencies in individual animals may inform future breeding decisions, though true genetic coagulopathies are rare in livestock.

Commonly co-occurring conditions with vitamin K deficiency depend on the underlying cause. Sweet clover poisoning in cattle occurs as an isolated condition specific to dicoumarol exposure. Dietary deficiency in poultry may be accompanied by other nutritional deficiencies when overall diet quality is poor. Animals with liver disease may have impaired clotting factor synthesis alongside any vitamin K-related issues. Intestinal diseases that impair fat absorption can affect multiple fat-soluble vitamins simultaneously. Animals weakened by blood loss from vitamin K deficiency are more susceptible to secondary infections and other opportunistic diseases.

Conditions with similar symptoms that must be differentiated from vitamin K deficiency include other causes of bleeding disorders and weakness. Thrombocytopenia from bone marrow disease, immune-mediated destruction, or consumption produces bleeding that may resemble vitamin K deficiency. Disseminated intravascular coagulation causes hemorrhage through complex mechanisms involving both clotting and anticlotting pathways. Inherited coagulation factor deficiencies, though rare, produce bleeding from birth. Rodenticide toxicity produces clinical and laboratory findings identical to vitamin K deficiency from sweet clover or dietary inadequacy. Vascular fragility from vitamin C deficiency, severe infections, or other causes can produce petechiae without coagulation abnormalities. Trauma-induced hemorrhage must be distinguished from spontaneous bleeding of coagulopathy.

Complications and sequelae of vitamin K deficiency relate primarily to the effects of hemorrhage on various organ systems. Anemia from blood loss may persist after coagulation is restored, requiring weeks for complete red blood cell regeneration. Hemorrhage into joints can cause permanent joint damage and chronic lameness. Central nervous system hemorrhage frequently results in death or permanent neurological deficits. Extensive soft tissue hematomas may become infected, requiring additional treatment. Adhesions from hemorrhage into body cavities can cause chronic digestive or reproductive problems. Animals that survive severe episodes may have prolonged recovery periods with reduced productivity during convalescence.