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equine hemodynamics
sgusvm
Question | Answer |
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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. |