Pathophysiology Case Study of Patient Mr Septica Sirs
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Question 1: In 400 words or less respond to the following statement
MrSeptica Sirs, 36 years of age, was admitted 3 days ago following a MVA with a haemo-pnuemothorax (treated with UWSD and now resolved), hypovolaemia (which has now resolved with appropriate IV fluids), IDC (removed yesterday), deep lacerations to knee (wound has been debrided in theatre and now dressed daily), head injuries treated with burr holes on Day 2. His temperature today at 1400hrs is 39.4°C.
- Mr Sirs has many risk factors for SIRS which does not necessarily have a bacterial focus. Some of the S/S of SIRS include: Hypovolaemia with decreased blood flow to vital organs, increased heart rate and stroke volume, acidosis, oliguria +/- anuria, peripheral oedema and Cardiogenic Pulmonary oedema.
- Mr SIRS who is at risk for Sepsis/SIRs should be administered Panadol for temperature above 38°C. In addition, at T38o appropriate cultures should be obtained of blood, wounds, IV sites, urine, and sputum. If cultures are negative the patient does not have SIRS or sepsis.
- Mr Sirs is due for the administration of an IVAB. One of his IV infusions is 0.9% Sodium Chloride. This infusion should not be switched off, the IV antibiotic should be administered with the concurrent infusion running at the prescribed rate and given over the time recommended. There is a risk however that further diluting the antibiotic decreases its therapeutic level.
Question 2: In 400 words or less respond to the following statement and provide supporting rationale.
Several weeks after the insertion of his tracheostomy tube, Mr Tic Tracky was diagnosed with pneumonia. He has a double cannula tube which comes with an outer and inner tube (which can be removed independently of the outer tube). You enter his room at 0800hrs and find him coughing weakly, he signals to you that he is having difficulty breathing (RR 34) and appears cyanosed. You would:
- Remove the inner tube and suction through the outer tube; provide 02 by tracheostomy tube mask and facial mask at 6-8L/min in between suctioning. Once he is breathing satisfactorily you will reinsert a new inner tube and reposition patient to facilitate optimum airflow. Also need to ensure the 02 administered via the tracheostomy tube is humidified.
- After clearing Mr Tic Tracky’s airway his Sa02 of 96% with a HB of 88mmol/L indicates adequate oxygenation and therefore no action required.
- After clearing Mr Tic Tracky’s airway the MO orders ABGs: Mr Tic Tracky’s Blood gases at this time of: Pa02 80mmHg, pH 7.30 PaC02 50mmHg, HC03 25mEQ/L show respiratory alkalosis related to the loss of C02 because of increased respirations.
Patients who are suffering with type II diabetes are studied to be at an elevated risk of acute renal failure, even if the risk factors are taken care of. This acute renal failure is more prominent in elderly patients and in those who are simultaneously suffering from other problems such as chronic disorders of kidney, congestive heart failure or high blood pressure.
In the event of acute renal failure, the basement membrane of the kidneys is damaged. The stiffening of the basement membrane causes changes in the pathology of cells of the mesangial and vascular region. The production of AGEs occurs; polyols collect through the aldose reductase reaction chain and the protein kinase C is stimulated. Other inflammatory pathways may also undergo activation due to the movement of the macromolecules causing secondary damage to the renal system. When the renal failure ensues in type II diabetes, glomerular hyperfiltration occurs causing intraglomerular hypertension. Next, in the course of renal damage microalbuminuria develops which eventually progresses to the condition of macroalbuminuria. Later, clinical deteriorations of the renal system may also cause albuminuria, edema, and nephrotic syndrome.(Evans & Capell, 2000)
Presence of microalbuminuria (30-300 mg albumin per day) can strongly confirm the presence of a cardiovascular disorder in patients with type II diabetes. The presence of protein in standard urinalysis tests depicts an already existing condition of macroalbuminuria.
Patients suffering from severe kidney disease show symptoms such as persistent fatigue, general ill feeling, the presence of headache, nausea, vomiting, poor eating, deep breathing pattern and swelling of the legs due to the presence of edema. The development of renal damage or subsequent renal failure is attributed to the presence of hypertension and poor control of blood sugar. In this case, consumption of unhealthy and fatty food, absence of a regular exercise and presence of urinary tract infection has played a significant role infurther damaging the kidneys. (American Diabetes Care, 2012)
Generally the renal damage in patients with type 2 diabetes progresses without any visible signs and symptoms of the condition. This patient has shown symptoms of urinary tract infection. In the last 4/7 days, she has complained of a decrease in urine output, drowsiness, fatigue and nausea all of which are indicative of acute renal failure.
Diabetic nephropathy occurs through a series of complex steps. Alterations in the hyperperfusion and hyperfiltration in the kidneys occur initially in the course of renal damage. This further helps in the progress to the release or outflow of albumin proteins from the capillaries in the glomerulus and bring about structural damage to the glomerulus such as thickening of the basement tissue, hypertrophy of the glomerulus, glomerulosclerosis, expansion of the mesangial cell and damage or destruction of the podocytes. These pathophysiologic mechanisms of the renal damage are responsible for signs and symptoms of acute renal damage. These clinical manifestations of the acute renal damage are a reduction in the rate of filtration of glomerulus and increase in the quantity if albumin being excreted. The most significant predisposing factors for acute renal damage have been reported to be poor control of glucose levels, increased blood pressure and cholesterol; all of which function in stimulating inflammatory mediators.
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