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Deteriorating Patient Suffering From Sepsis

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Question:

Develope a Profile of a Patient Presenting to a Health Care facility with Sepsis.
 
 

Answer:

Introduction:

Mr. A, a 70 year old male was admitted to emergency department by his son. His son told nurse that 15 days back he was cutting vegetables in their garden and accidently he cut his fingure. He carelessly washed the bleeding fingure, covered it with small piece of cloth and continued working. Next day, he removed piece of cloth from fingure and observed that wound was open and it was moist. After two days, fingure was swollen and red. He visited nearby physician. Physician prescribed him with broad spectrum antibiotic, however he discontinued it after two days. On the arrival in the emergency department, his son explained that Mr. A is having high fever and he is behaving like confused person since last two days. His history indicates that he is suffering through cancer since last two years and type 2 diabetes mellitus since last ten years. Currently, he is on the medications like metformin for type 2 diabetes mellitus and cisplatin for cancer. In the initial assessment, it was observed that his vital signs are deviating from normal values. His temperature was 40.2 ?C, his respiratory rate was 25, his blood pressure was 86/62 mmHg and pulse rate was 114.  Blood culture identified E. coli infection. All these information indicate he has developed septic shock. For initial management, he was given appropriate antibiotic and kept on ventilation.

Definition and two diagnostic criteria:

Sepsis is defined as devastating response of body to the infections which may lead to the tissue damage, organ failure and consequently death of the person (Singer et al., 2016). In the initial assessment, it was observed that Mr. A has increased pulse rate (114) and increased breathing rate (25). These are the prominent symptoms of sepsis. In sepsis due to coronary dysfunction there is insufficient blood flow. This insufficient blood flow leads to the increased pulse rate and respiratory rate. Due to less blood flow there is reduced blood pressure in the patient with septic shock. Due to less circulating volume of blood, there is less venous return. When blood gets ejected from the heart, elastic fibers present in the arteries are helpful in maintaining high pressure gradient. This high pressure gradient is due to the expansion of arteries for accommodation of blood and again they recoil. This sequence of expansion and recoiling is measured as pulse rate. If cardiac output is more and systolic pressure is high, then pulse is strong. In case of septic shock there is less cardiac output and low systolic pressure. It indicates weak pulse. This weak pulse increases its frequency to maintain normal pressure in the blood vessels. Thus, in septic shock patients pulse rate is rapid due to less circulating blood and hypotension (DellaVolpe et al., 2015). This less circulating blood also leads to the pulmonary complication. Due to less circulating blood, there is less oxygen supply to the tissues. Due to less oxygen supply to the tissues oxygen desaturation occurs. Due to oxygen desaturation, there is decreased amount of oxygen and increased amount of carbon dioxide in the blood. For proper functioning of tissues and organs, optimum level of oxygen is required in the blood. Lung tries to maintain this normal level of oxygen through respiration. Lung put extra efforts to inhale oxygen and exhale carbon dioxide. As a result there is increased respiratory rate in patients with septic shock. In this case arterial blood gas (ABG) test should be performed in patients with hypoxia. This test measure pH, oxygen and carbon dioxide level in the blood. ABG test evaluate capability of lung to transfer oxygen to the blood. Less supply of blood to the tissues is termed as hypo-perfusion and it is due to hypovolemic shock. Common symptoms of hypovolemic shock are hypotension, rapid heart rate (tachicardia) and dizziness. Due to less supply of oxygen to the cells and tissues, there is lactic acid fermentation in the cells. It leads to the accumulation of lactate in the cells which is termed as lactic acidosis (Kim and Hong, 2016; Gajic et al., 2011).       

 

Assessment in emergency department:    

Complete blood cell (CBC) count and differential count was performed in Mr. A. This test gave estimation of red blood cell, white blood cell, hemoglobin and platelets. This test gave idea about infection in Mr. A. Test for serum electrolyte levels was carried out. Renal and hepatic function tests were carried out to understand functioning of kidney and liver. Kidney function test was carried out by blood tests for urea and creatinine levels. Hepatic function test was carried out by blood test for alanine aminotraseferase (ALT) and aspartate aminotraseferase (AST). Coagulation status in Mr. A was evaluated by calculating prothrombin time and activated thromboplastin time. Amount of oxygen, carbon dioxide and acidity were measured by applying arterial blood gas analysis. This test was performed because respiratory rate in Mr. A was increased due to hypoxia. Serum lactate test was performed to assess hypoperfusion in Mr. A. Due to less cardiac output, there is possibility of hypoperfusion of tissues in Mr. A. Urine analysis and culturing of urine sample were performed to detect urinary tract infection. Blood culture was performed to detect presence of microbial infection in Mr. A. This test was useful for the initiation of the antibiotic therapy based on the type of detected bacteria (Reinhart et al., 2012; Khardori, 2014).

Initial interventions:

Antibiotic therapy was initiated in Mr. A immediately within 1 hr of diagnosis of septic shock. Initial therapy was started with broad spectrum antibiotic without waiting for detection of specific microorganism. Levofloxacin was administered because of its usefulness in gram positive and gram negative bacteria. It is also useful in cases of pneumonia.  Later, it was observed that Mr. A was detected with E.coli infection. After detection of E.coli infection, Mr. A was administered with third generation cephalosporin like ceftriaxone (Yealy et al., 2014).

 


Mr. A developed respiratory distress due to septic shock. This respiratory distress is due to the diffuse alveolar damage, acute lung injury and mild acute respiratory distress syndrome. Mr. A had rapid breathing rate due to hypoxemia. Hence, Mr. A requires intubation and mechanical ventilation for optimum respiratory support. This ventilation was considered in the initial phase after diagnosis of septic shock. Supplemental oxygen was given to Mr. A though oxygen mask with flow rate of 2 l/min. Ventilation was provided with suitable sedation because it reduced work of breathing in Mr. A. As a result, it reduces metabolic demand for breathing in case of Mr. A. Low tidal volume was kept at the time of artificial ventilation because it reduces, alveolar overdistention and repetitive opening and closing of alveoli at the time of artificial ventilation. This collapse of alveoli was prevented by applying positive end-expiratory pressure (PEEP) (Ranieri et al., 2012; Yealy et al., 2014).  

Pathophysiology and assessment:

Pathophyiology of septic shock is very complex and it is not completely understood. Inflammation and coagulation plays prominent role in the pathophysiology of septic shock in response to the infection. Gram-positive bacteria are the major cause of septic shock followed by gram-negative bacteria and fungal infections. Circulating proteins in the body interacts with infected microbial proteins. It leads to the chain of events which results in the release of both proinflammatory and anti-inflammatory mediators. In the event of inflammatory phase complement system also get activated. Mediators of the complement system produces endothelial damage and hypotension. Due to infection and flowed by inflammation there is increase release of acute phase inflammatory mediators like C-reactive protein, proinflammatory cytokines like tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6), markers for nitric oxide production like plasma methemoglobin and nitrite/nitrate concentrations (Cinel and Opal, 2009).

Cardiopulmonary changes are the prominent changes occur is septic shock. Initial phase is the vasodilatation phase which is termed as warm shock. In this phase there are warm extremities, little systemic resistance, elevated or optimal cardiac output, optimal or lesser blood pressure and elevated pulse pressure.

Reduced venous return in the early phase of sepsis lead to increased level of catecholamines. This lead to the increased adrenergic response and consequently cardiac contractibility and heart rate. In progressive sepsis, mitochondrial dysfunction and tissue hypoxia occurs which lead to the decreased levels of adenosine triphosphate formation. This inequality between demand and supply of oxygen lead to cardiac myocytes death. This results in the cardiac dysfunction and there is increased levels of troponin, reduced contractibility, weakned ventricular response to fluid, ventricular dilation and hypotension. In this phase, there is increased capillary permeability which results in the loss of intravascular fluid to the interstitial space. As a result, there is loss of intravascular fluid. Later phase is the vasoconstricted phase in the septic shock. This phase is marked with cold extremities, hypotension, little pulse pressure and reduced cardiac output. In this phase there is reduced myocardial contractibility, loss of intravascular fluid and peripheral vasoconstriction (Schuetz et al., 2011). 

TNF-α produced due to infection and inflammation is responsible for the decrease in myocardial function. TNF-α also produces vasodilatation and decrease in the cardiac contractibility. This action occurs due to the increase in the cGMP level due to the increased nitric oxide production (Kothari et al., 2012). Peripheral oxygen supply is reduced in the patients with septic shock due to less circulating blood. Lung would not be able to exchange enough oxygen at the capillary–alveoli interface. This results in the hypoperfusion at the tissue level. Due to less oxygen at the tissue level, lung initiates compensatory mechanism. Bu virtue of this compensatory mechanism, lung starts breathing at the faster rate to supply more amount of oxygen to the lungs. Hence, in septic shock patients there is increased breathing rate.  

Assessment findings indicating patient is safe:

For the transfer of the patient to the ward two clinical conditions were identified as indicators of safety of Mr. A. These conditions were blood pressure and respiratory rate. After initial treatment to Mr. A, it was observed that his blood pressure and respiratory were improved. His measured blood pressure was 116/78 and respiratory rate was 18 breaths per minute. There was improvement in the breathing rate in Mr. A because he kept on the ventilation with oxygen supplementation. Due to this, his oxygen saturation level improved. His Po2 level observed was 93 %. As result, his lung needS not to breathe faster to deliver more amount of oxygen to the blood and tissues. His pulmonary function test also was performed. This pulmonary function test includes spirometric measurement of expiratory reserve volume (ERV), forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), forced expiratory flow 25% to 75% (FEF25-75), functional residual capacity (FRC), residual volume (RV), peak expiratory flow (PEF) and total lung capacity (TLC) (Gold and Koth, 2016; Scanlon, 2016). Measurements in these tests were normal. Blood pressure measurement for Mr. A was performed using sphygmomanometer. There was recovery in the hypotension because infection in Mr. A was recovered. As a result, there was less secretion of inflammatory mediators and nitric oxide. Less release of nitric oxide increased blood pressure from hypotension to normal level (Kothari et al., 2012).

Findings indicating patient is detoriating:

Deteriorating conditions observed in Mr. A were disturbed mental status, impaired renal function and impaired hepatic function test. Renal output was measured in Mr. A in previous 18 hours. It was observed that no urine was passed in previous 18 hours and it was measured less than 0.5 ml/kg/hour with the help of catheter. Glomerular filtration rate was very less in Mr. A. According to literature urine output is variable in patients with less glomerular filtration rate. It can vary for oliguria to high urine output. It reflects urine output is not solely dependent on glomerular filtration rate, however it depends on difference between glomerular filtration rate and rate of tubular reabsorption. Decreased urine output mainly occurs due to dehydration, kidney failure, hypovolemic shock, multiple organ dysfunction syndrome and urinary tract infection (Dennen et al., 2010). Out of these kidney failure, hypovolemic shock and urinary tract infection were observed in Mr. A.  Hepatic function test can also get affected in patients with septic shock. Hepatic function was assessed by performing blood tests for ALT and AST. Hepatotoxicty reflects reduced metabolic capability of Mr. A. This reduced metabolic activity leads to the improper digestion of the consumed food and impaired elimination of waste products. This impaired elimination lead to the accumulation of toxic waste in body. This toxic waste material adversely affects proper functioning of the body. Adult patients with septic shock generally develop depression, stress and anxiety. Mr. A also exhibited symptoms related to mental disorder. This may be due to improper functioning of the organs and difficulty in normal living. Mr. A is confused about his thoughts and he developed memory loss. He was also facing problem in sleeping because of stress (Mayr et al., 2010; Iwashyna, 2010).

 

Inotropic therapy  (Management) :

In septic shock, systemic infection leads to the hypotension. This hypotension is unresponsive to the fluid resuscitation. Along with infection control, initial management goal of the septic shock patient is to maintain normal blood pressure and cardiac output. In unusefulness of fluid resuscitation, vasopressor or inotropic therapy can be effectively used to maintain optimum hemodynamic condition (Dellinger et al., 2012). Several studies were carried out for the effectiveness of vasopressors like norepinephrine, dopamine, epinephrine, vasopressin, phenylephrine and inotropes like dobutamine, milrinone. Role of vasopressor agents in the septic shock is to improve blood pressure. Norepinephrine stimulate α-adrenergic and β-adrenergic receptors thereby increasing vasoconstriction, cardiac contractibility and heart rate. Dopamine stimulate dopaminergic receptors and increase renal perfusion. Norepinephrine and dopamine are considered as the first line therapy for septic shock, however use of norepinephrine is more because of its fewer side effects. Moreover, effect of norepinephrine is stronger and consistent as compared dopamine.  Epinephrine is used as alternative to the norepinephrine and acts by same mechanism. Epinephrine increases arterial blood pressure, cardiac output and vascular tone. One study indicates that epinephrine has more side effects as compared to the norepinephrine. Patients treated with epinephrine exhibited more lactic acidosis and tachycardia. Vasopressin produces actions like vasoconstriction, adrenocorticotropin hormone release and water retnetion. Vasopressin also activated oxytocin receptors which induces vasodilatation. Some studies indicated that vasopressin is useful in reducing dose of norepinephrine (Vasu et al., 2011; De Backer et al., 2012). Vasopressin also increase creatinine clearance and urine output. Most of the research indicated that vasopressin is a rational second line therapy for septic shock in patients where nonepinephrine is ineffective. Inotropic agents can be used alone or along with existing vasopressors. Dobutamine is useful in to relieve signs of hypoperfusion. 

 

Invasive monitoring:

Pulmonary artery catheterization was used for obtaining hemodynamic information of Mr. A. It is a flow directed and balloon shaped catheter. This catheter is mainly useful for investigating complications due to acute myocardial infarction. Cardiac output can be measured using pulmonary artery catheterization by application of thermodilution technique. Gold standard for measuring cardiac output is electromagnetometry of aortic blood flow. In studies, it has been found that pulmonary artery catheterization exhibited good correlation with electromagnetometry. In septic shock patients continuous monitoring of cardiac output is very necessary. Hence, pulmonary artery catheterization can be effectively used in septic shock patients because it is a simple measurement technique, it provides calibrated continuous cardiac output, pulmonary artery pressure, pulmonary artery occlusion pressure and mixed-venous oxygen saturation (Velissaris et al., 2016).       

Conclusion:

Mr. A, a 70 year male was admitted to emergency department with the complain of fever and confused state. Description by his son revealed that he might develop infection due to cut in his fingure. However, he discontinued it after consumption for short span. Preliminary evaluation revealed that he had E.coli infection. Also, his vital signs like temperature, respiratory rate, blood pressure and pulse rate indicated that he had septic shock. In the emergency department, preliminary treatment was initiated for him. This treatment comprises of antibiotic treatment and supplementation of oxygen through ventilation. After preliminary treatment, it was observed that his condition was improving and he was more stabilized as compared to the earlier condition. Normal values obtained for blood pressure and respiratory rate were considered as safe parameters for transfer to ward from emergency department. In septic shock, there are more chances of multiple organ dysfunctions. In Mr. A also psychological, renal and hepatic dysfunction was observed. It indicates his condition was detoriating. Inotropes and vasopressors can be effectively used in the management of septic shock patient. In summary, condition of septic shock patient detoriates very rapidly and careful monitoring and management required in these patients.

ISBAR Handover: 

Introduction

Myself Ms. B, Residential Nurse in Emergency Department to head of Ward.

Patient is Mr. A, Age - 70yrs., male admitted to Dr. Z in emergency department.

Situation

Mr. A was admitted to emergency department with fever and confused state of mind. Now he is stabilized and need to transfer to ward for further monitoring.

Background

Mr. A is suffering through septic shock due to infection in the fingure. He was having fever, high pulse rate, low blood pressure and high pulse rate. History of cancer and type 2 diabetes mellitus. He is on medications like metformin, cisplatin and ceftriaxone.

Assessment

Blood pressure and respiratory rate were measured after treatment with ceftriaxone. There is improvement in both the parameters.

Recommendation

We need to send Mr. A to ward for further monitoring.

 

 

References:

Cinel, I., and Opal, S.M. (2009). Molecular biology of inflammation and sepsis: a primer. Critical Care Medicine, 37(1), 291-304.

Dellinger, R.P., Levy, M.M., Rhodes, A., Annane, D., Gerlach, H., Opal, S.M., et al. (2013). Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Critical Care Medicine, 41(2), 580-637.

DellaVolpe, J.D., Moore, J.E., and Pinsky, M.R. (2015). Arterial blood pressure and heart rate regulation in shock state. Current Opinion in Critical Care, 21(5), 376-80.

Dennen, P., Douglas, I.S., Anderson, R. (2010). Acute kidney injury in the intensive care unit: an update and primer for the intensivist. Critical Care Medicine, 38(1), 261-75.

De Backer, D., Aldecoa, C., Njimi, H., and Vincent, J.L. (2012). Dopamine versus norepinephrine in the treatment of septic shock: a meta-analysis. Critical Care Medicine, 40(3), 725-30.

Gajic, O., Dabbagh, O., Park, P.K., Adesanya, A., Chang, S.Y., Hou, P., et al. (2011). Early identification of patients at risk of acute lung injury: evaluation of lung injury prediction score in a multicenter cohort study. American Journal of Respiratory and Critical Care Medicine, 183, 462–470.

Gold, W.M., and Koth, L.L. (2016). Pulmonary function testing. In: Broaddus VC, Mason RJ, Ernst JD, et al, eds. Murray and Nadel's Textbook of Respiratory Medicine. 6th ed. Philadelphia, PA: Elsevier Saunders.

Iwashyna, T.J., Ely, E.W., Smith, D.M., and Langa, K.M. (2010). Long-term cognitive impairment and functional disability among survivors of severe sepsis. Journal of the American Medical Association, 304(16), 1787-94.

Khardori, N. (2014).  Sepsis: Diagnosis, Management and Health Outcomes. Nova Science Publishers .

Kim, W.Y., and Hong, S.B. (2016). Sepsis and Acute Respiratory Distress Syndrome: Recent Update. Tuberculosis and respiratory diseases, 79(2), 53–57.

Kothari, N., Bogra, J., Kohli, M., Malik, A., Kothari, D., Srivastava, S., et al. (2012). Role of active nitrogen molecules in progression of septic shock. Acta Anaesthesiologica Scandinavica,  56(3), 307-15. 

Mayr, F.B., Yende, S., Linde-Zwirble, W.T., Peck-Palmer, O.M., Barnato, A.E., Weissfeld, L.A., et al. Infection Rate and Acute Organ Dysfunction Risk as Explanations for Racial Differences in Severe Sepsis. Journal of the American Medical Association, 303(24), 2495-2503.

Ranieri, V.M., Rubenfeld, G.D., Thompson, B.T., Ferguson, N.D., Caldwell, E., Fan, E., et al. (2012). Acute respiratory distress syndrome: the Berlin Definition. Journal of the American Medical Association, 307(23), 2526-33. 

Reinhart, K., Eyrich, K., and Sprung, C. (2012). Sepsis: Current Perspectives in Pathophysiology and Therapy. Springer Science & Business Media.

Scanlon, P.D. (2016).  Respiratory function: mechanisms and testing. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine. 25th ed. Philadelphia, PA: Elsevier Saunders.

Singer, M., Deutschman, C.S., Seymour, C.W., Shankar-Hari, M., Annane, D., Bauer, M., et al. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). Journal of the American Medical Association, 315(8), 801-10. 

Schuetz, P., Jones, A.E, Aird, W.C., and Shapiro, N.I. (2011). Endothelial cell activation in emergency department patients with sepsis-related and non-sepsis-related hypotension. Shock, 36(2), 104-8. 

Vasu, T.S., Cavallazzi, R., Hirani A, et al. (2011). Norephinephrine or Dopamine for Septic Shock: A Systematic Review of Randomized Clinical Trials. Journal of Intensive Care Medicine, 27(3), 172-178.

Velissaris, D., Karamouzos, V., Kotroni, I., Pierrakos, C., and Karanikolas, M. (2016).  The Use of Pulmonary Artery Catheter in Sepsis Patients: A Literature Review.  Journal of Clinical Medicine Research, 8(11), 769–776.

Yealy, D.M., Kellum, J.A., Huang, D.T., et al. (2014). A randomized trial of protocol-based care for early septic shock. New England Journal of Medicine, 370(18), 1683-93.

 

 

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