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equine hemodynamics

sgusvm

QuestionAnswer
The most common causes of acute blood loss in the horse are trauma, surgical procedures and guttural pouch mycosis (erosion of the carotid artery).
External hemorrhage is immediately obvious, but hemorrhage into a major body cavity may be occult (ie spontaneous rupture of middle uterine artery, splenic rupture, neoplasia, etc).
Hemoperitoneum may induce signs of colic.
hemothorax likely results in dyspnea.
Acute massive blood loss induces hypovolemic shock characterized by tachycardia, tachypnea, cold extremities, pale mucous membranes, muscle weakness and eventual death from cardiovascular collaspe.
Diagnosis of acute blood loss is based upon clinical signs, evidence of hemorrhage, and anemia accompanied by hypoproteinemia.
Initially, no change in the PCV or total protein level, however, rapid mobilization and redistribution of the ECF volume to maintain circulating volume results in decline of PCV/TP over 12 – 24 hours following the acute loss of blood.
Severity of blood loss may be masked by splenic contraction induced by activation of the sympathetic nervous system in response to blood loss. Bone marrow response to blood loss
In horses, erythroid regeneration is limited to evidence of mild anisocytosis w/ variable increases in mean corpuscular (MCV). Hemoperitoneum and hemothorax may be visualized as fluid with the respective body compartment by ultrasonographic examination, but confirmation requires
Initial treatment of acute blood loss requires immediate intervention to control hemorrhage.
For traumatic wounds, arterial blood vessels should be clamped or ligated if possible.
internal hemorrhage that is unable to be controlled, general anesthesia may not be advisable given the cardiovascular status of the bleeding patient, as it is difficult to identify the source of internal hemorrhage in many cases.
The second goal is provision of prompt and adequate fluid therapy, which depends largely upon whether or not hemorrhage can be controlled.
In the patient w/ controlled hemorrhage (i. distal limb laceration with ligation of peripheral arterial vascular trauma), hypovolemic shock should be treated by aggressive administration of intravenous crystalloid solutions at 40-80 ml/kg body weight.
Administration of 4ml/kg hypertonic saline (7pctNaCl) may temporarily reverse the pathophysiologic state of shock as well as provide anti-inflammatory effects which may be beneficial in cases of severe trauma. It is useful to consider a
The clinical response to fluid administration should be evaluated in light of ongoing losses to assist determination of the amount of replacement volume necessary.
In the patient where hemorrhage is unable to be controlled (ie hemoabdomen from rupture of middle uteren artery) aggressive fluid resuscitation cannot be justified.
When hemorrhage is incontrollable fluid protocols can exacerbate bleeding as a result of increases in blood pressure, disruption of clots, and hemodilution of clotting factors.
A protocol of controlled hypotension resuscitation should be followed when hemorrhage is uncontrollable.
Hypotensive resuscitation involves low volumes of crystalloids or whole blood to maintain organ vitality without normalizing blood pressures.
The goal of mean arterial pressure 60mmHg should provide perfusion of organs without disruption of hemostasis.
If anemia becomes life-threatening whole blood transfusion may be necessary.
When the PCV falls to less than 20pct following acute blood loss RBC reserves have likely been depleted.
If the PCV falls less than 12pct or less in 24–48 hours blood transfusion is indicated in most cases.
In contrast to the patient with a low, but stable, PCV between 12-20pct which may not require transfusion.
In addition to PCV, other transfusion triggers should be considered before the decision for blood product administration is made.
Use of heart rate, blood lactate, indirect blood pressure and colloid oncotic pressure should also be evaluated.
Blood transfusion should be considered only a temporary therapeutic measure as the majority of the transfused RBCs will be removed from circulation by the reticuloendothelial system within 2–4 days of transfusion, even with confirmation of major and minor crossmatch.
The cross-matching procedure serves to alleviate life-threatening severe anaphylactic reaction to donor blood, but because of the high degree of blood type polymorphism the equine species displays, the donated RBCs experience a shortened life span in the recipient host.
The first transfusion of whole blood to a horse is usually well-received (provided the horse has not been previously transfused, pregnant or sensitized by immunization) as the level of natural alloantibodies is low and only weakly reactive.
It is the patient that requires multiple transfusions or that received a potentially incompatible transfusion that develops alloantibodies rapidly, which make subsequent transfusion hazardous to the health of the recipient.
When planning a transfusion, replacing 20-40pct of blood loss should be sufficient to sustain life until the bone marrow can respond.
As an example, if a 500kg patient suffers blood loss to drop the PCV from 36 to 12, this represents a loss of 27L of blood (considering the patient has 8 body weight in blood volume 40L).
Administration of colloid fluid / blood products should not be administered >20ml/kg/h and the recipient patient should be monitored very closely during transfusion for indication of transfusion reaction (ie piloerection,incTPR, musle fasciculations, defecation, restlessness, or sudden collapse in severe cases).
If evidence of transfusion reaction occurs, the transfusion should be discontinued, the patient treated with anti-inflammtory therapy and administered IV crystalloid fluid.
The transfusion may be inititated again very slowly at a later time point.
One of the most common causes of acute blood loss in horses is trauma. Use of transabdominal and transthoracic ultrasound will
External wounds should be clamped, ligated or pressure-bandaged until the animal may be transported to a surgical facility.
Guttural pouch mycosis is another primary cause of acute blood loss in horses, which is invariably fatal unless the primary disease is treated. Guttural pouch mycosis is a
Fungal invasion of the neurovascular structures coursing through the walls of the guttural pouches results in clinically apparent disease. Although the exact cause of guttural pouch mycosis is not known, a number of fungi, especially
Guttural pouch Lesions are mostly unilateral, but may be seen bilaterally with the most common presenting complaint of intermittent epistaxis and dysphagia.
Epistaxis results from fungal erosion of the wall of the internal carotid artery in the roof of the medial compartment.
The external carotid and maxillary arteries may also, but less commonly, be affected.
Epistaxis may be unilateral or bilateral as the pharyngeal openings to the guttural pouch are caudal to the nasal septum.
Episodes of epistaxis occur at rest and may be intermittent but culminating in fatal hemorrhage.
Diagnosis is made via endoscopy of the guttural pouch to confirm the diptheritic lesion within the pouch.
Pathogenesis and predisposing factors are unknown in guttural pouch epitaxis.
Both medical and surgical treatments are available, but surgical intraarterial occlusion of the affected vessels is considered the most effective.
Both balloon tipped catheterization and arterial coils have been used.
It is necessary to occlude the affected artery both proximally and distally, encouraging thrombus formation, to prevent collateral circulation from the Circle of Willis from reperfusing the pouch.
Once the blood supply is removed the fungus will die.
Medical treatment is aimed at topical treatment of the fungal lesions by way of the pharyngeal openings of the guttural pouches.
Variable success has been achieved by placing fungicidal and fungistatic drugs, topical enzymes and organic iodine compounds into the guttural pouch.
This may be a frustrating disease to treat due to the additional accompanying neurologic dysfunction (dysphagia, blindness, Horner’s syndrome) but also because recurrent fungal plaques have been observed.
The chance of fatal hemorrhage is possible as long as fungal plaques are present within the guttural pouch.
An additional cause of acute blood loss is hemothorax or hemoabdomen.
The cause of the intraabdominal hemorrhage is identifiable in only 78pct of cases.
the most common cases of hemoperitoneum resulting from traumatic rupture of the spleen, reproductive tract hemorrhage in mares, and neoplastic lesions.
It appears there may be some breed association (Arabs and Thoroughbreds) as well as an age association (middle age to older horses >13 years) in equine patients diagnosed with hemoabdomen.
The most common clinical signs of hemoabdomen include colic, lethargy, hypovolemic shock, pale mucous membranes, prolonged CRT, tachycardia and tachypnea,anorexia, reluctance to move, weakness, trembling, cool extremities, and abdominal distention.
Abdominal ultrasonography yields a characteristic picture of fluid swirling in the abdomen.
Primary goals of therapy include treating hypovolemic shock by restoring perfusion and oxygen delivery to tissues, correcting fluid deficits, preventing further blood loss and preventing associated complications.
Controlled hypotension may be necessary until appropriate internal hemostasis has been achieved.
These patients should be kept calm (acepromazine)and in a quiet environment and not be forced to move.
Blood transfusion is indicated with severe life-threatening anemia.
The uses of both anti-fibrinolytics and pro-coagulants have been described, but as yet, there are no efficacious studies to support their use.
Short-term outcome is primarily related to the underlying cause, with survival rates varying between 51–74pct.
Created by: alljacks