Pathophysiology of the Nervous System - Essay Example

? Case Scenario The case emerges from a situation when a 78- year old male starts behaving abnormally in a local restaurant and is reported as being in a highly agitated condition. He is seen pacing up and down, bearing a restless and agitated demeanor, and seems to be unable to sit still though the staff members of the restaurant and the friends of the person were trying to settle him down. The patient is named Jack. He gives an impression of a disorientated person and from his behavior, it is clear that he does not want anybody to touch him. Still, Jack has certain degree of self-awareness, which is visible in the fact that he somewhat recognizes that the medical practitioner was there to help him. But he is found not to be able to answer the questions put to him coherently. He is speaking in a stream of words and is referring to the world as screwed up. He suddenly stops talking and goes quite while standing unsteadily on his feet. He also states that he desperately wants to call his sister. As the situation suggests, he may be suffering from Sepsis, or Thyrotixicosis. The patient is displaying symptoms of a neurological disorder. This paper will be carrying out a diagnosis review of the patient focusing on the pathophysiology of the condition involved. It will also provide a detailed justification for the diagnosis. Topics under consideration are the symptoms, their causes, the potential consequences of the condition, and also the short-term and long-term medical intervention strategies. The age of Jack, the medication that he is under, his health history, the implications of this newly displayed condition, his possibility of recouping normalcy and the specific medical interventions required will be elaborately dealt with in this paper. While some primary scrutinizing was being done to observe Jack's vital signs, it became perceivable that his agitated state was getting more unmanageable. This being the scenario, this writer will provide a differential diagnosis on the health status of the nervous system of the given person, approaching the problem from a pathophysiological point of view. It is clear that the patient is agitated, but it is not yet the stage of diagnosis to suggest that what the patient exhibit is rthe sign of an organic condition. Mohr et al. (2005) have pointed out that the key symptoms of agitation are, “motor restlessness, increased responsiveness to external or internal stimuli, irritability, [and] inappropriate and usually purposeless verbal and motor activity” (p.327). The patient under scrutiny is displaying all these symptoms. The major medical causes of agitation are “thyrotoxicosis, encephalitis, meningitis, Sepsis, brain trauma, dementia, delirium, [and] seizure disorders” (Ng. et al., 2010, p.47). Another category of causes include “intoxication (alcohol, cocaine, methamphetamine), [and] alcohol withdrawal” (Ng. et al., 2010, p.47). Agitation is a condition defined from the view-point of pathophysiology as “a nonspecific constellation of relatively unrelated behaviors that can be seen in a number of different clinical conditions, usually presenting a fluctuating course” (Lindenmayer, 2000, p.5). The causative pathophysiological elements are a brain dynamics emerging out of “dysregulations of dopaminergic, serotonergic, noradrenergic, and GABAergic systems” (Lindenmayer, 2000. P.5). In other words, agitation could be pathophysiologically an expression of “specific neurotransmitter dysregulations” (Allen, 2002, p.119). Differential diagnosis In order to carry out a differential diagnosis, the practitioner needs to collect information on the history of the patient, to examine and talk to the patient to take note of the “vital signs” (Binder and McNiel, 1999, p.1553), and undertake a “physical examination and laboratory work” (Binder and McNiel, 1999, p.1553). Carrying out an accurate diagnosis of agitation is a difficult venture (Cardinal and Bullmore, 2011, p.151). This is especially the case when the patient is unable to “communicate clearly” (Cardinal and Bullmore, 2011, p.151). The symptoms of this patient include agitation, illegible speech, imbalance while walking, inability to concentrate, inability to recognize familiar people, inability to recognize one's own physical condition and location, and a depressed mental state. Based on an initial review of the case and knowing from Jack's friends about the general health history of the patient, it can be assumed that Jack is either suffering from Sepsis or Thyrotoxicosis. An exhaustive examination including collecting information on patient health history, hereditary disease history, and subsequent laboratory examinations could only provide conclusive information that can lead to accurate diagnosis of the patient's condition. Differential diagnosis: 1) Sepsis 2) Thyrotoxicosis Obtaining history Regarding this patient, the most prominent neurological condition is his “incoherent speech” (Allen, 2002, p.126). As a few of his friends are present in the restaurant, they can be interviewed to formulate a general health picture of the patient (Allen, 2002, p.126). The friends might be knowing whether the patient has any previous medical history, including respiratory infection, abdominal pain, and joint pain, as these could be signs leading to a diagnosis of Sepsis (Snyder, Kivlehan and Collopy, 2012). To make the diagnosis precise, the witnesses, and the staff of the restaurant can be asked some questions to know about the subtle aspects of the behavior of the patient after entering the place (Sublette, Nachbar, and Hao, 2006, p.499). While interviewing Jack, specific questions are to be asked, “to determine the number and quality of agitation-induced behaviors, such as emotional liability, confusion, memory loss, hyperactivity and hostility” (“Rapid Assessment”, 2003, p.12). The patient also has to be asked about “his current diet and known allergies [prevailing] illnesses, [and] drug history” (“Rapid Assessment”, 2003, p.12). Vital signs An initial diagnosis of the patient indicates a serious pathophysiological problem. A “very acute onset of symptoms” is evidence to an underlying pathopsychology (Allen, 2002, p.126). Signs exhibited by this patient that suggest a pathophysiology include, “fluctuating levels of consciousness, [and] disorientation to time and place”, symptoms that are proven elements of pathophysiology-driven agitation (Allen, 2002, p.127). To make the diagnosis accurate, the vital signs have to be taken note of in regular intervals (Sublette, Nachbar, and Hao, 2006, p.499). A lactate monitor can also be used to confirm a diagnosis of Sepsis (Snyder, Kivlehan and Collopy, 2012). Physical and mental status examination The physical and mental status examination of the patient will only be partially possible owing to the condition of the patient and also his inability to co-operate (Allen, 2002, p.121). The patient needs to be interviewed, and this has to be preferably done in a “quiet, nonstimulating setting” (Glick, Berlin, Fishkinder and Zeller, 2008, p.118). The practitioner also has to be careful about the potential for violent behavior as “most violence that is not premeditated is preceded by a prodrome, often 30 to 60 minutes in duration, of increasing psychomotor agitation, such as pacing or loud speech” (Glick, Berlin, Fishkinder and Zeller, 2008, p.118). But as regarding to this particular patient, there being no imminent danger of violence, the practitioner has to attempt an interview to collect as much information as possible (Glick, Berlin, Fishkinder and Zeller, 2008, p.118). It is necessary that a “basic neurologic assessment for future comparison” is made (“Rapid Assessment”, 2003, p.12). Stress-producing factors have to be avoided by ensuring “adequate lighting”, creating a peaceful ambiance, and giving the patient sufficient time to relax and if needed, get some sleep as well (“Rapid Assessment”, 2003, p.12). Diagnosis-1 – Sepsis: Pathophysiology The symptoms of Sepsis have been delineated by Remick (2007) as follows. Two or more of the following symptoms have to be confirmed to make a diagnosis of Sepsis, “Body temperature >38°C or 90 beats per minute, (…) Respiratory rate >20 breaths per minute or arterial CO2 tension less than 32 mm Hg or a need for mechanical ventilation (…) (and) White blood count greater than 12,000/ mm3 or 10% immature forms” (Remick, 2007, p.1436). The patient in question was showing the symptoms (1), (2) and (3) and hence the possibility of the condition being Sepsis is high. The patient is also having severe dehydration when examined and this also points to a diagnosis of Sepsis (Snyder, Kivlehan and Collopy, 2012). Sepsis is considered as an alarming clinical condition as every year in the world, many patients die of this condition (Remick, 2007, p.1435). One earlier definition of Sepsis was that it is a Systemic Inflammatory Response Syndrome caused by an infection (Remick, 2007, p.1435). The current definition is a broader one including four characteristics, namely, 1) a predisposition caused by co-morbidities, 2) an infection, 3) a Systemic Inflammatory Response Syndrome which is a response to the infection, and 4) “organ dysfunction” (Remick, 2007, p.1435). It is the patients having abnormal inflammation responses and abnormal neutrophil responses who are at high risk of dying from Sepsis (Remick, 2007, p.1435). The major problem faced by Sepsis patients is the “life-threatening alterations in their coagulation system” (Remick, 2007, p.1435). Sepsis, as a pathophysiological condition, is a complex process that is manifest as an “unbalanced interaction between the body’s inflammatory and anti-inflammatory responses to an invading microbe” (Snyder, Kivlehan and Collopy, 2012). When a microbe enters the body breaching the defensive mechanism of the skin, namely, epithelial border, a set of responses are initiated (Snyder, Kivlehan and Collopy, 2012). There is a host of body agents that recognize this breach and they are, “host neutrophils, macrophages, mast cells and other cells of the immune system, including natural antibodies” (Snyder, Kivlehan and Collopy, 2012). These cells in turn produce chemical mediators known as cytokines (Snyder, Kivlehan and Collopy, 2012). Cytokines “activate the local inflammatory response, resulting in increased capillary permeability and blood flow, which in turn allows neutrophils (phagocytes) to access the infected tissue, crossing from circulation into the interstitial space” (Snyder, Kivlehan and Collopy, 2012). Neutrophils will eventually “ingest” microbes (Snyder, Kivlehan and Collopy, 2012). This process gets manifest as “anti-inflammatory, procoagulant and thermoregulatory actions” and when there is an imbalance in returning to normalcy, the Sepsis condition results, causing “a relative hypovolemia, and an increase in systemic microvascular permeability” (Snyder, Kivlehan and Collopy, 2012). This will in turn lead to “edema formation through third-spacing of fluids” (Snyder, Kivlehan and Collopy, 2012). This could lead to a lung condition that is described as acute respiratory distress syndrome (ARDS) (Snyder, Kivlehan and Collopy, 2012). The third spacing of fluids will cause reduction in blood flow, and to compensate this, the heart will start to beat faster (Snyder, Kivlehan and Collopy, 2012). This is described as a “hyperdynamic state” and if the condition persists, a hypotension situation will happen (Snyder, Kivlehan and Collopy, 2012). At the early stage of Sepsis what happens is, “Derangements in the normal distribution of blood volume contribute to the development of tissue and organ hypoxia” (Snyder, Kivlehan and Collopy, 2012). Eventually, “when tissues and organs lack access to adequate oxygen, they will convert to anaerobic metabolism that will result in a metabolic acidosis from elevated lactate and other acids” (Snyder, Kivlehan and Collopy, 2012). In order to cope with this, “respiratory alkalosis develops as the patient increases their respiratory rate in an effort to blow off the accumulating acids in the blood in the form of carbon dioxide” (Snyder, Kivlehan and Collopy, 2012). It has to be noted that “despite the increase in respiratory rate, hypoxia can develop secondary to a ventilation-perfusion mismatch that occurs as a result of the derangements in blood distribution” (Snyder, Kivlehan and Collopy, 2012). When early Sepsis progresses to a more severe condition, there will also be further complex bodily reactions. The physiological changes include, “a coagulation imbalance”, moving ahead “to the clinical condition of disseminated intravascular coagulation (DIC)” (Snyder, Kivlehan and Collopy, 2012). Further, “DIC leads to clot formation in the microvasculature, and the result is thrombosis of these vessels, with impaired tissue perfusion” (Snyder, Kivlehan and Collopy, 2012). In an intense effort “to control these multiple small clots”, the body will “overproduce(...) and disperse(...) anticoagulants” (Snyder, Kivlehan and Collopy, 2012). It is observed that “the downward spiral of DIC can progress rapidly as more clots form in response and then are also dissolved” (Snyder, Kivlehan and Collopy, 2012). What will happen eventually is, “platelets and clotting factors are consumed, and diffuse bleeding leading to petechiae and purpura will develop” (Snyder, Kivlehan and Collopy, 2012). If proper attention and correction is not made available, “end-organ failure to the heart, lungs, kidneys and liver will ensue” (Snyder, Kivlehan and Collopy, 2012). Global tissue hypoxia caused by reduced supply of oxygen is yet another co-morbidity of Sepsis (Rivers, McIntyre, Morro and Rivers, 2005). Thyrotoxicosis: Pathophysiology The condition of thyrotoxicosis is characterized by a condition where “inappropriately high tissue thyroid hormone” causes a set of bodily discomforts (Bahn, Burch, Cooper, Garber, Greenlee, Klein, Laurberg, McDougall, Montori, Rivkees, Ross, Sosa and Stan, 2011, p.e2). The causes of this condition could be Graves’ disease, toxic multinodular goiter and toxic ade-noma (Bahn et al., 2011, p.e3). The physical examination of the patient of Thyrotoxicosis has to include, “measurement of pulse rate, blood pressure, respiratory rate, and body weight [and] […] thyroid size; presence or absence of thyroid tenderness, symmetry, and nodularity; pulmonary, cardiac, and neuro-muscular function […] [and] presence or absence of peripheral edema, eye signs, […] [and] pretibial myxedema” (Bahn et al., 2011, p.e7). This patient though having high pulse rate and respiratory rate, there is no visible symptoms of blood pressure, and Jack is also having sufficient body weight. The patient is also not showing symptoms of edema, eye signs, and the thyroid gland also looks and feels at touch, normal. Hence the possibility of Thyrotoxicosis can be ruled out. A serum TSH test also showed negaitve evidence as to the patient having Thyrotoxicosis (Bahn et al.,2011, p.e7). Intervention options Paramedical interventions Sepsis requires different types of care according to the severity of this medical condition. Though this patient is not showing acute symptoms of Sepsis, hospitalisation might be required. It has been observed that in “otherwise healthy patients, over-the-counter medications or prescription medications from physicians may be sufficient” (Snyder, Kivlehan and Collopy, 2012). Yet the graduation of mild sepsis to severe sepsis and septic shock can happen in a few hours and hence early diagnosis is very important (Rivers, McIntyre, Morro and Rivers, 2005). As there is no recent history of trauma or surgeries, the Sepsis can be considered as mild (Snyder, Kivlehan and Collopy, 2012). Yet, as the elderly people are at higher risk when it comes to this condition, it is suggested that after certain period of medication and monitoring, the patient be shifted to a hospital if there is any worsening of the situation (Snyder, Kivlehan and Collopy, 2012). Pre-hospital interventions have to include, “ensuring that there is an open airway and adequate ventilation and oxygenation” (Snyder, Kivlehan and Collopy, 2012). If any breathing problem is found, oxygen has to be administered using nonrebreather mask (Snyder, Kivlehan and Collopy, 2012). Tubing and ventilation also might be needed (Snyder, Kivlehan and Collopy, 2012). Clinical interventions Option-1 Early antimicrobial therapy can be administered in the early stages of Sepsis as is the case with this patient (Rivers et al., 2005). This is also an important intervention strategy because when antibiotics under this therapy are taken by the patient at the earliest, the possibility of worsening of the situation including death has been found to be highly reduced (Rivers et al., 2005). It is the best practice to start administering antibiotics within one hour of the diagnosis (cited in Rivers et al., 2005). The drug combinations have to be decided based on the source of infection and also the personal drug resistance patterns (Rivers et al., 2005). Option-2 Glycemic control in the form of “intensive insulin therapy” has been found to be effective in treating this condition in acutely affected patients (Remick, 2007, p.1441). This therapy is used to keep blood sugar levels below 8.3 mmol/L (Orford, 2006). While doing this therapy, there is a risk of the patient slipping into a state of hypoglycaemia (Orford, 2006). Hence while carrying out this therapy, the effort will be to achieve the “lowest glycaemic range” all the same “avoiding hypoglycaemia” (Orford, 2006). Option-3 Another effective intervention strategy has been “early goal-directed therapy” in which “early administration of fluids and blood products” will improve the condition of the patient (Remick, 2007, p.1441). The major steps in this treatment include, “1) early identification of patients with sepsis; 2) optimization of oxygenation, ventilation and circulation; 3) initiation of drug therapy, including vasopressors and antibiotics; and 4) controlling the source of infection” Snyder, Kivlehan and Collopy, 2012). It has been found that this intervention method is helpful in reducing mortality rates as compared to traditional methods (Snyder, Kivlehan and Collopy, 2012). The administration of fluids has to be following a precise schedule. It is observed that “patients with severe sepsis may require 2 liters or more of an isotonic crystalloid during their initial therapy (first 30–60 minutes), and may receive as much as 6–10 liters within the first 24 hours of treatment” (Snyder, Kivlehan and Collopy, 2012). The fluid has to be administered fast (Snyder, Kivlehan and Collopy, 2012). The recommended infusion rate is, “as fast as 0.5 liters every 5–10 minutes as needed to restore adequate perfusion (as measured by a systolic blood pressure of 90 mmHg or a mean arterial pressure greater than 60 mmHg)” (Snyder, Kivlehan and Collopy, 2012). It is also cautioned that “even in patients for whom you’d normally consider withholding it, such as in those with renal or congestive heart failure”, there is no other way than to administer “aggressive fluid volume replacement” (Snyder, Kivlehan and Collopy, 2012). The medication generally include, “dopamine, dobutamine and norepinephrine” (Snyder, Kivlehan and Collopy, 2012). These are vasopressor agents that can bring back the arterial pressure to normal (Rivers et al., 2005). Among these drugs, dopamine could worsen tachycardia, a condition that the patient might already would have been suffering from, and hence the other two drugs are preferred (Rivers et al., 2005). Epinephrine can also be administered if the patient is unresponsive to the other drug mentioned above (Rivers et al., 2005). As the patient might be loosing body temperature, artificial warming should be given (Snyder, Kivlehan and Collopy, 2012). Insulin therapy will have to be used to keep blood sugar levels normal (Snyder, Kivlehan and Collopy, 2012). Early goal-directed therapy has been found to reduce mortality rates in cases of Sepsis by 16.5 percent (Rivers et al., 2005). Option-4 Intropic therapy can be used as a treatment option when the patient is suffering from a myocardial suppression (Rivers et al., 2005). The drug, dobutamine is administered in this therapy in which Rivers et al. (2005) have observed that “inotropic support with dobutamine may improve myocardial depression, but may also unmask underlying hypovolemia because it acts to increase contractility and reduce peripheral vascular resistance.” Rivers et al. (2005) has revealed that “as ventricular compliance and contractility respond, CVP will decrease as the stroke volume improves.” It is also stressed, “further fluid replacement may be required to maintain CVP at 8– 12 mm Hg. Dobutamine is then titrated at increments of 2.5 ?g/kg/min every 20–30 minutes to a ScvO2 measurement of 70%” (Rivers et al., 2005). To avoid tachycardia, dobutamine can be replaced with Milrinone but this drug can cause harm to kidney (Rivers et al., 2005). Option-5 When ventilation is given to the patient, owing to stretching of lung tissues, there is the risk of lung injuries and it is to prevent this, an optimal tidal volume strategy is adopted (Rivers et al., 2005). Evolving intervention strategies Treatment options like administering “vasodilators, high-volume hemofiltration and corticosteroids” are at the experimental stage (Rivers et al., 2005). The use of nitroglycerin to improve blood pressure abnormalities and microcirculatory flow of blood is also found to be effective in some studies (cited in Rivers et al., 2005). Hemofiltration will be helpful in removing cytokines that cause the inflammation and corticosteroids can improve chest condition (Rivers et al., 2005). These strategies of course are at trial stage and needs to be extensively researched in order to be brought into clinical practice. Conclusion The best strategy so far been evolved for treating Sepsis and Septic shock is, “evidence-based recommendations”, and the best recommendation available is “early goal-directed” therapy within six hours of identification of the disease (Dellinger et al., 008, p.1). Timely attention and care being an important factor, and keeping in mind, the age of Jack, hospitalization can be the safest option. Goal-directed therapy has to be initiated as soon as the patient is hospitalized and there should not be any delay in starting treatment. References Allen, M.H. 2002. Emergency psychiatry, Ameircan Psychiatric Publishing, Arlington, VA. Bahn, R.S., Burch, H.B., Cooper, D.S., Garber, J.R., Greenlee, M.C., Klein, I., Laurberg, P., Binder, R.L., and McNeil, D.E. (1999) 'Emergency psychiatry: Contemporary practices in managing acutely violent patients in 20 psychiatric emergency rooms', Psychiatric Services, vol. 50, no.12, pp.1553-1554. Cardinal, R.N. and Bullmore, E.T. 2011. 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