The Pathophysiological Process - Case Study Example

Trauma case study Name Institution Pathophysiological process presented by patient signs-Hypovolemic shock-hemorrhagic The patient presents signs of hypovolemic shock. Hypovolemic shock results from loss of blood fluid which subsequently lead to organs failure since there is inadequate circulating fluid volume and perfusion. The endothelium is known to play a very critical role in vascular and reparative processes. Therefore the endothelium is highly affected by the hypovolemic shock. The effect of the endothelium by the hypovolemic shock is as a result of ischemia related to endothelial cells. Also, the reperfusion resulting from fluids resuscitation. Hypovolemic shock shocks are caused by the deprived oxygen and also the endothelial cell apoptosis. In other cases, the hypovolemic shock is secondary to the hemorrhagic shock. That is an acute external blood loss and GI bleeding disorder. Hemorrhagic can also result from acute internal bleeding in the abdominal cavities and thoracic cavities ("Traumatic hypovolemic shock", 2010). Human body activate the major physiological system such as renal, hematologic, cardiovascular and neuroendocrine systems as a way of responding to the acute hemorrhage. The hematologic system activates the cascade coagulation as a way of responding to the acute severe blood loss it is responsible for the contraction of bleeding vessels by releasing the local thromboxane A2. The platelets are also activated by the release of local thromboxane A2; the resultant is an immature clot on the bleeding source. Collagen is exposed from the damaged vessels that form fibrin deposition that makes clotting stable ("Traumatic hypovolemic shock", 2010). The cardiovascular system increases the heart rate as a way of responding to hypovolemic shock. Also, the peripheral blood vessels constrict while myocardial contractility increase. The response occurs as a result of the release of norepinephrine and the reduction of the baseline vagal tone, which is regulated by aortic arch, pulmonary vessels, left atrium and carotid arch baroreceptors. In other words, the cardiovascular system will respond to the hypovolemic shock by redistributing blood to the vital organs such as the brain, kidneys and the heart, while redistributing blood from the muscles, GI tract, and the muscles. Renal system stimulates the secretion of renin from the juxtaglomerular apparatus as a way of responding to the hemorrhagic shock. The secreted renin help convert the angiotensinogen to angiotensin I. the angiotensin I am later converted by the lung and liver to angiotensin II. Angiotensin II has two major effects that help in reserving the hemorrhagic shock. It enhances the arteriolar smooth muscle vasoconstriction, it also stimulates the secretion of the aldosterone in the adrenal cortex (Hobson, 2013). Consequently, the aldosterone assist the reabsorption of sodium and water conservation. On the other side, the neuroendocrine system increases the antidiuretic hormone circulating. The antidiuretic hormone is produced by the pituitary gland it helps in decreasing the blood pressure and also reduce the sodium concentration. The antidiuretic hormone increase the water and salt reabsorption through the distal tubule, loop of Henle and collecting ducts. The abnormal signs such as the BGL-4.2mmol/L, blood pressure -70/45mmHg and temperature at 35.5 degrees Celsius are outside normal ranges because, reduced blood pressure due to massive loss of blood through the wound that shows the femur. Therefore the amount of pressure exerted by the arteries wall is reduced due to the less blood remaining in the system. The skin looks pale due to the redistribution of the blood from the muscles and skin to the brain, heart, and kidneys (Hobson, 2013). The BGL is affected by the interrupted rate of absorption of nutrients in the body tissues. The pulse is also weak thus related to the low blood pressure. The typical signs of hypovolemic are pale, anxious skin and weak pulse. Patient management and treatment A kind of procedural treatment should be given to the patient to be to manage the condition. For instance, ventilation is supposed to be provided to the patient. In our case, the patient is in a decompensated shock since the pulse is hardly heard. Therefore 100% oxygen should be provided using the facial mask that is non-breathable. Before the transportation, to the hospital, the patient limbs and neck spine are supposed to be immobilized. The main agenda of hypovolemic shock treatment is the correction of hypotension. Thus the fluid deficit replacement is paramount, fluids such as Colloids- dextran, Albumin, Hetastarch, and Pentastarch. Crystalloids-ringer lactate, isotonic saline (0.9% NaCl). Blood products such as packed blood cells, fresh frozen plasma, and whole blood transfusion. Products that boost normal blood functioning, for example, the prothrombin complex, tranexamic acid, and recombinant human factor VIIa. Medication of hypovolemia- the patient can be given the vasoconstrictors medicine to increase the blood pressure. Note that the drug is not supposed to be given before the correction of hypovolemia using fluids. Other medicines include norepinephrine, epinephrine, high dopamine doses, milrinone, dobutamine, phenylephrine, and isoproterenol. Pathophysiology of spinal cord injury The patient suffered a spinal cord injury that is it is probable that the stab touched the spinal cord and affected the nervous that stretches to the left abdomen and left leg. The numbness is justifying that the patients’ spinal cord and nerves were affected. The spinal cord injury may rise from 1 to 2 levels of spinal in hours or days of the injury. The pathophysiological of the spinal cord injury is biphasic such that it occurs both in primary and secondary phase. In primary phase, the mechanical injury is involved where the spinal cord fails due to dislocation or fracture of the spinal cord. Thus distracting the blood vessels, axon and cell membranes (Yılmaz, 2014). The primary phase is followed by the secondary phase that comprises ischemia, inflammation, edema, electrolyte shifts, delayed apoptotic cell death and free radical production. The neurological deficits are experienced immediately after initial injury while the protracted tissues destruction occurs after the secondary phase. The spinal cord injury may be as a result non-traumatic and traumatic. The non-traumatic cause is related to the compression of cord, bone metastasis or cancer. While the traumatic spinal cord injury results from penetrating injury. So in our case, the spinal cord injury is traumatic since the patient was stabbed in the back. Spinal cord injury is associated with the spinal shock (Claydon, Steeves, & Krassioukov, 2005). The shock is considered to be a complete loss of the neurologic functions that is rectal tone and reflexes. The spinal shock is a transient physiologic that affects the reflex depression of the cord function under the level of injury. The case is associated with loss of functions of the sensorimotor. Flaccid paralysis affecting the abdomen and bladder is present. Although the symptom last for few hours or days and the reflex arcs begins to function again. The patient suffers from incomplete cord syndrome which is recorded when there exist a complete motor and loss of the sensory functions below the injury level. The incomplete cord syndrome comprises of central cord syndrome, interior cord syndrome and brown-sequard syndrome. The blood pressure which is 80/40mm Hg is low thus abnormal due to the loss of external loss of blood. The condition of the skin that is pale, cool and diaphoretic show that the patient may have lost blood through internal and external bleeding. The low blood pressure can also be attributed by probable internal bleeding. The numbness on the left side of the abdomen and left leg was as a result of the probable loss of neurologic functions. Preliminary diagnosis that justifies the pathophysiology The numbness of the lower left abdomen and left leg show the disruption of the nervous activities in T6 or thoracic vertebrae above the T6. Numbness is signifying a lack of sense to pain. Low blood pressure also signifies probable internal bleeding since the external bleeding was not severe. The state of the skin which pale, cool and diaphoretic show that the patient had lost a lot of blood the resulted to the redistribution of the blood from the skin and muscle to the brains, kidney, and heart. Management and treatment of spinal cord injury. To manage the neurogenic shock, the patient could receive the replacement of the judicious fluid with the crystalloid isotonic solution, so as to maintain the oxygenation and also perfusion. Mechanical oxygenation may also be required as a supplemental. Note that the crystalloid solution to be administered should not exceed 2L (Claydon, Steeves, & Krassioukov, 2005). Overzealous crystalloids can result to pulmonary edema since the patients are risked to acute respiratory distress syndrome. Spinal cord injuries can be managed through the circulation, respiration and airway precedence. Treatment and management of the neurogenic shock should ensure that blood pressure is at 90/100mmHg, the oxygenation and perfusion of the injured spinal cord are maintained, heart beat rate is at 60-100beats in a minute and also prevent hypothermia. Also both the complete and incomplete injuries patients can be administered with the steroids to improve the motor strength in muscles for function provision. However, the steroids should be administered within the eight hours of the injury. Also, the methylprednisolone 30mg/kg should be administered over 15minute. The treatment also involves maintaining supplementary oxygen and thoracostomy. Surgical intervention is also another way of treating spinal cord injury in cases where the spinal cord is dislocated, neurologic deterioration or in the case of locked facets.   References Claydon, V., Steeves, J., & Krassioukov, A. (2005). Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology. Spinal Cord, 44(6), 341-351. http://dx.doi.org/10.1038/sj.sc.3101855 Hobson, M. (2013). Pediatric Hypovolemic Shock. The Open Pediatric Medicine Journal, 7(1), 10-15. http://dx.doi.org/10.2174/1874309901307010010 Traumatic hypovolemic shock. (2010). Nursing, 40(10), 39-40. http://dx.doi.org/10.1097/01.nurse.0000388309.52898.d7 Yılmaz, T. (2014). Pathophysiology of the spinal cord injury. Journal Of Clinical And Experimental Investigations, 5(1), 131-136. http://dx.doi.org/10.5799/ahinjs.01.2014.01.0378 Read More