Sepsis/Systemic Inflammatory Response Syndrome (SIRS) - Advanced Pathophysiology and Health Assessment
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Sepsis/Systemic Inflammatory Response Syndrome (SIRS)
Advanced Pathophysiology and Health Assessment
This case study aims to provide a detailed analysis of the clinical manifestations of sepsis, supported by the pathophysiological process behind each manifestation. This will be achieved through a case study involving an actual patient who was admitted to the intensive care unit (ICU). For the purpose of this paper, the patient will be known by the pseudonym Mrs. Morris. This case will discuss Mrs. Morris’ demographic details considering her presenting problem and medical history. The pathogenesis and pathophysiology of sepsis will be discussed, and the aetiology and predisposing factors in relation to the case will be determined. Identification of the clinical manifestations will be achieved through the use of a primary and secondary survey, further diagnostic investigations will then be examined and evaluated. Also discussed are psychosocial, ethical and legal issues in relation to the case.
Prior to her admission, Mrs. Morris was staying in a nursing home. She had a cerebrovascular accident (CVA; also known as stroke) in 2002 with residual R sided weakness and paresthesia, myocardial infarction (MI) in 2000 and peripheral vascular disease (PVD).
Mrs. Morris is an 82-year old frail woman living in a nursing home in Melbourne. Mrs. Morris is a widow with no child. Her only relative that visit her occasionally in the nursing home is her married niece. She had a heart attack (MI) in 2000 and had stroke (CVA) in 2002. She also has residual R sided weakness, paresthesia and PVD. All these health problems led to her becoming bed-ridden. Health problems associated with old age and her health condition such as pneumonia and pressure ulcer led to sepsis.
On admission, the patient underwent primary assessment and resuscitation. Since the patient presents multiple health conditions and she was suffering from Sepsis, assessment and resuscitation were of the utmost importance.
The secondary survey was also carried out – employing haemodynamic monitoring, Haemodynamic monitoring is performed to provide the clinician with a greater understanding of the pathophysiology of the problem being treated than would be possible with clinical assessment alone. Heamodynamic monitoring is done to accomplish three things:
· To establish a precise health-related diagnosis
· To determine appropriate therapy
· To monitor the response to the therapy (Elliot et al, 2007).
Invasive heamodynamics monitoring was employed in order to fully assess the state of the patient. Haemodynamic monitoring is a head to toe monitoring approach (Urden et al 2006). During this stage, deterioration of Mrs. Morris’ haemodynamic status occurred and the patient required oxygen at 8L via Hudson mask, and an 8 hourly 1L flask of N/Saline IV. An indwelling urinary catheter was also used to collect regular urine sample from the patient. Diagnostic procedures were performed when Mrs. Morris became stable.
Initial Assessment and Resuscitation
For the case of Mrs. Morris, it is important to initiate fluid resuscitation, especially because she was dehydrated. The patient was suffering from infection – pneumonia and stage 3 pressure ulcer. Because of this, she required intensive care unit (ICU) management. Health history was also investigated in order to identify the source(s) of sepsis and identify the risk factors that may affect outcome (Garibaldi & Diallo, 2009). The patient is at risk of infection because of the indwelling catheter. The patient’s infections were also reviewed in order to guide initial antibiotic therapy.
Mrs, Morris was admitted into an ICU bed. One concern is that she has a level 3 pressure ulcer which needs intense medical attention. The room must also be cleaned thoroughly since the patients age and health condition makes her susceptible to infections. The patient has pneumonia and sepsis which requires close monitoring. The patient was also dehydrated. The patient was closely monitored by the staff. Strict ICU procedures and guidelines were followed to ensure the safety of the patient and the staff. The bedding as well as the position of the patient was carefully planned because she is suffering from level 3 pressure ulcer. The patient was assessed and resuscitated using the ABCDE approach which means:
· A – airways assessment; maintenance and oxygen
· B – breathing and ventilation assessment
· C – circulation assessment; intravenous (IV) access and fluids
· D – disability; assess the neurological status and check the blood glucose
· E – exposure and environmental control (Kirk, 2000)
The patient required a Hudson mask since she was suffering from pneumonia and sepsis because she required higher concentrations of oxygen (Cooper, et al 2006). It is important to repeatedly assess the patient’s airways because her condition makes her at risk to respiratory failure.
The patient was hyperventilating and displayed shortness of breath. Patient laboriously breathing, respiratory rate was 38 breaths per minute.
Patient was in a fevered state. Heart rate was 88 beats per minute. Blood pressure was 98/62. Lower pH (7.27). PaCO2 is within the normal range. HCO3 was 18 mmol/L. The blood gas assessment findings point to mixed respiratory and metabolic acidosis (Gennari, 2005).
Sleepiness, confusion, anxiety, disorientation, and agitation were observed in the patient. The patient then became unconscious.
The patient is put in the Intensive Care Unit in order to carefully monitor the patient’s vital sign measurements which include temperature, pulse, blood pressure, respiratory rate, oxygen saturation, consciousness level and urine output. A fluid balance chart is used.
Central Nervous System
· Mrs. Morris was septic
· Has history of CVA
· Has hypoxia according to AGB result
· Patient was drowsy, confused or unconscious
· Unable to move limbs
· Pupils were equal and reactive to light
· Glasgow Coma Scale 11
· Temperature 38.1 Degrees Celsius
· Mrs. Morris has oxygen at 8L Hudson mask
· Patient has lung parenchymal problem (pneumonia)
· Respiratory rate 38 breaths per minute, labored, using accessory muscles
· Oxygen saturation is 60%
· Decreased delivery of oxygen required delivery of 60% oxygen
· Peripheral cyanosis
· Arterial Blood Gas (ABG): ph of 7.27, PCO2 of 44 mmHg, PO2 of 32 mmHg, HCO3 of 18 mmol/L, Base Excess of neg 7.3 mmo/L. These results indicate hypoxia and patient needs to be intubated.
· Patient been diagnosed Pneumonia, so might hear moist rales on auscultation, decrease air entry, dullness sound might present on percussion
· Decreased cardiac output
· BP 98/62, HR 88 and regular, due to the past history of MI, 12 lead ECG might reveal ischemic change
· CVC need to be inserted for rehydration and medication administration, and monitoring CVP level
· Arterial line should be inserted to monitor BP and ABG.
· Patient has CVA, and has stage III pressure ulcer, which means patient could lie on the bed most of the time
· Because of immobilization, patient could have the problem of constipation
· Glucose: 31.3 mmol/L
· Patient does not have DM problem but stressed
· Illness can cause blood sugar to rise
· Indwelling urinary catheter (IDC) insitu
· Site of IDC is clean, no redness, swelling or discharge visible
· As the pathology results, patient has UTI
· Antibiotics should be given to treat UTI
· Pressure ulcer
Pathogenesis and Pathophysiology
Sepsis begins with the invasion and growth of microorganisms (gram-positive, gram-negative, fungal, or viral) in a normally sterile tissue space (Parsons & Wiener-Kronish, 2003).
Infection is the most common causes of sepsis, however, in many sepsis patients the infectious etiology is not identified. The same biochemical and physiological changes as those seen with infectious agents may also present in other non-infectious conditions, such as pancreatitis, trauma, or extensive burns. It was once thought that the response to the initial insult or triggers precipitated a cascade of events where interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF) played a central role. With our current greater understanding of the inflammatory cascade, we now know that that sepsis is caused by an imbalance in the normal inflammation and coagulation responses of the patient. On the one hand, cytokines IL-1, IL-6, and TNF-a alter the secretion of hormones, which in turn direct an increase in the resting energy expenditure: amino acids are exported from the muscles to the liver, gluconeogenesis increases, and a catabolic state is created. On the other hand, these cytokines cause increased neutrophil activation, and directly damage organs by activating the coagulation cascade and inhibiting fibrinolysis. This leads to diffuse endovascular injury, and can lead to multiorgan dysfunction and death.
Aetiology and Predisposing Factors
Mrs. Morris was particularly susceptible to sepsis because of different factors such as immune system compromise due to old age, increased number of comorbid illnesses, and residence in nursing home facilities (Vincet, et al 2002). The fact that Mrs. Morris has a history of cerebrovascular accident (CVA; also known as stroke) in 2002 with residual R sided weakness and paresthesia, myocardial infarction (MI) in 2000 and peripheral vascular disease (PVD), predisposes her to acquiring infections. Mrs. Moriss also has pneumonia and stage III pressure ulcer and is dehydrated, making the risk of sepsis greater.
In the case of Mrs. Morris, before being infected with sepsis, the patient was already suffering from a stage III pressure ulcer. A pressure ulcer according to Hess (2007) is a localized site of cell death that occurs most commonly in areas of compromised circulation secondary to pressure. These ulcers may be superficial, caused by local skin irritation with subsequent surface maceration, or deep, originating in underlying tissue. Deep ulcers may go undetected until they penetrate the skin. Pressure ulcers are most likely to develop in patients who experience sustained pressure over bony prominences. Patients who spend most or all of their time in a bed or alternative seating device such as a wheelchair without shifting their body weight properly are a great risk. Risks increase with various cofactors, such as partial or total paralysis. At stage III, Mrs. Morris exhibits full-thickness tissue loss. Subcutaneous fat visibility. Slough is also present but it does not obscure the depth of tissue loss. Pressure ulcer was probably caused by the patient’s health condition. The patient suffered a cerebrovascular accident in 2002, which inhibited her movements. The patient’s frail state also increased the risk of pressure ulcer since she spends most of her time in bed.
The pathogenesis of sepsis is exceedingly complex and involves an interaction between multiple microbial and hosts factors (According to (Norton et al, 2008), sepsis is a clinical syndrome manifested as deleterious host response to an infectious process (Irwin & Rippe, 2008). The risk of disseminated infection and sepsis following the onset of tissue invasion by pathogens from initial site of injury varies markedly depending on the type of infection, location and degree of tissue invasion, and the intrinsic virulence of the causative pathogen. The likelihood of developing multi-organ dysfunction, hemodynamic compromise, and lethal septic shock after infection begins is heavily dependent on the antimicrobial defense capacity and fundamental nature of the individual host response to microbial challenge.
Risk Factors for Older Patients
Aging is a process associated with numerous risk factors that contribute to the increasing incidence of, and mortality from, severe sepsis.
A number of aging processes lead to poorer performance status, an independent predictor of mortality:
• disuse atrophy from an inactive life-style
• sarcopenia from accelerated muscle loss
• changes in responsiveness to trophic hormones
(growth hormones, androgens, and estrogens)
• neurological alterations
• altered cytokine regulation
• changes in protein metabolism
• changes to dietary intake
Older patients are often nutritionally or immunologically impaired, making them an easy target for infection and its associated complications. They are frequently affected by comorbidities that require treatment with foreign devices (e.g. indwelling urinary catheters, gastrostomies, cystostomies, tracheostomies, peripherally inserted catheters) that make patients vulnerable to infections or complications. The natural barriers of innate immunity are broken, providing increased access for pathogens. There is also evidence of abnormal T and B cell function in older patients , although the response to infection appears to elicit a normal expression of proinflammatory cytokines.
One of the physiological changes of aging includes a substantial decrease in olfactory discrimination by age 70; sweet, sour, bitter, and salty tastes are impaired, which contributes to a decreased enjoyment of meals, aggravating the anorexia of aging. An older patient’s nutritional status can also be affected by:
• inadequate funds or resources
• mobility and transportation issues
• social isolation
• functional limitations
• poor or restricted diets
• chronic disease
• poor dentition
• alcohol or substance abuse
The medical community is in need of an improved understanding of how drug absorption, hepatic metabolism, and drug responses vary with old age. It is evident that drug clearance from the body, particularly through renal mechanisms, is altered in aging persons. Age-related decline in renal function predominately underlies the decreased drug clearance. Because the kidneys are largely responsible for the excretion of several antibiotics, dose adjustments and monitoring of serum drug levels may be necessary for certain drugs in older patients. Testing only blood creatinine levels could underestimate or overestimate the renal function of these patients, and therefore creatinine clearance would be a better assessment of their kidney’s functional capacity.
Institutionalization (e.g. nursing homes) is common amongst older people, who have to go through a period of adjustment to their new environments. Adequate social support should help them through the process easily, and minimize the associated problems, such as depression, crowding, and neglect, all of which have impact on nutrition and immunity.
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