PREPARED BY: TINTU VARGHESE ICU DEPARTMENT PREPARED BY: TINTU VARGHESE ICU DEPARTMENT.
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Transcript of PREPARED BY: TINTU VARGHESE ICU DEPARTMENT PREPARED BY: TINTU VARGHESE ICU DEPARTMENT.
CASE NO: 195937NAME: XYZ AGE:25YRSSEX: MALEDIAGNOSIS: ACUTE RESPIRATORY DISTRESS SYNDROM, SEPTECEMIA
DOA:05/02/2013
DEMOGRAPHIC DATA
The patient is 25 years of age, male, approximately weighs 80kg
He is unconscious with ET tube with ventilator support and patient is sedated. GCS3/15,with the following vital signs.
BP=130/80, PR=70bpm, RR=24mts
Temp= 38.2, SPO2= 93%
GENERAL ASSESSMENT
CHEST AND LUNGS
Equal chest expansionDecreased air entryBilateral wheezing sound presentBilateral crept present
25yres male patient came in ER with complaints of tachypnea, agitated, SOB, fever, productive cough which was started one week ago and became worse. From
ER patient was confused, SPO2 was low 85%,CXR showed patchy opacities are seen in the middle and lower zone of both lung . Hilar shadows and vascular markings are prominent in both lungs. Mild to moderate pleural effusion in both lungs
PRESENT MEDICAL HISTORY
Patient was shifted to surgery ward, patient was desaturated and developed tachypnea and shifted to ICU for further treatment and observation. Patient was intubated and on ventilator and fully sedated .patient developed hypotension and started inotropic support for two days. After all management patient was extubated and fully conscious and oriented. Patient shifted to surgery ward.
DRUG DOSE ROUTE ACTION
INJ. COLOMYCIN
1MILLION IV ANTIBIOTICS(generation3cephalosporin)
INJ.TAVANIC 750MG IV ANTIBIOTICS(generation2 fluoroquinilone)
INJ. MEROPENEM
1GM IV ANTIBIIOTICS(generation3 cephalosporines)
INJ. NEXIUM 40MG IV H2RECEPTOR
INJ. PERFALGAN 1GM IV ANTIPYRETICS
TAB TAMIFLUE 75MG NGT ANTIVIRAL
MEDICATIONS
TEST PATIENT VALUE
NORMAL VALUES
WBC 42.25% 4.23-9.07%
HGB 13.2(G/DL) 13.7-17.5(G/DL)
PLT 346(10^3/UL) 163-337(10^3/UL)
UREA 8.7mmol/L 1.8-8.3 mmol/L
CREATININE 113.7 mmol/L 58-110 mmol/L
SODIUM 142 mmol/L 135-150 mmol/L
INVESTIGATION
POTTASIUM 3.8 mmol/L 3.5-5 mmol/L
PT 13.6SEC 10.9 TO 16.3 SEC
INR 1.31% 2 -4%
APTT 29.6SEC 27-39SEC
PH 7.13 7.35-7.45
PO2 88.8 80-100
PCO2 58.5 35-45
CHCO3 19.4 mmol/L 22-26 mmol/L
Patchy ( air space) opacities are seen in the middle and lower zone of the both lungs.
Hilar shadows and vascular markings are prominent in both lungs.
Mild to moderate plural effusion in both lungs.
X-RAY CHEST ( CHEST AP VIEW)
BIilateral pleral effusion ( large amount)with opacity is seen in lower area of both lungs
ULTRASOUND CHEST
A distinct type of hypoxemic respiratory failure characterized by acute abnormality of both lungs was first recognized during the 1960s. Military clinicians working in surgical hospitals in Vietnam called it shock. Then referred to it as adult respiratory distress syndrome . Subsequent recognition that individuals of any age could be afflicted led to the current term, acute respiratory distress syndrome (ARDS).
INTRODUCTION
ARDS is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue . Clinical hallmarks of ARDS are hypoxemia and bilateral radiographic opacities, while the pathological hallmark is diffuse alveolar damage (ie, alveolar edema with or without focal hemorrhage, acute inflammation of the alveolar walls, and hyaline membranes).
Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid resulting in severe dyspnea, hypoxemia and diffuse pulmonary infiltrates.
DEFINITION
lobes:
superior lobeinferior lobe
Direct Lung Injury◦Common causesAspiration of gastric contents or other substances.
Viral/bacterial pneumonia
ETIOLOGY AND RISK FACTORS
Chest traumaEmbolism: fat, air, amniotic fluid
Inhalation of toxic substancesNear-drowningO2 toxicityRadiation pneumonitis
Less common causes
◦Less common causes Acute pancreatitis Anaphylaxis Prolonged Cardiopulmonary bypass
surgery Disseminated intravascular coagulation Multiple blood transfusions Narcotic drug overdose (e.g., heroin) Non pulmonary systemic diseases
Less common causes
◦ restlessness◦ Dyspnea◦ Low blood pressure◦ Confusion◦ Extreme tiredness◦ Change in patient’s behavior
Mood swing Disorientation Change in LOC
◦ If pneumonia is causing ARDS then client may have Cough Fever
EARLY SIGNS AND SYMPTOMS
◦Shortness of breath.◦Tachycardia◦Cyanosis (blue skin, lips and nails)◦Think frothy sputum◦Metabolic acidosis◦Abnormal breath sounds, like crackles◦ Increased PaCo2 with respiratory alkalosis.◦Severe difficulty in breathing i.e., labored,
rapid breathing.◦ Decreased PaO2
LATE SIGNS AND SYMPTOMS
PATHOPHYSIOLOGY
Lung injury
Release of Vasoactive substances (serotonin, histamine, bradykinin)
Damaged Type II alveolar cell
Surfactant production Alveolocapillary
membrane permeability
Vascular narrowing & obstruction
AlveolarCompliance and recoil
Bronchoconstriction
Outward migration of blood cells & fluids
from capillaries
Atelectasis
Pulmonary EdemaHyaline membrane
formation
Lung compliance
Impairment in gas exchange
ARDSPulmonary
hypertension
24 hours vital signs observed will be monitored and documented. Monitor for exhaustion and signs of reduced lung compliance eg:
use of accessory muscles for respiration. Evaluate effectiveness of respiratory function like rate, rhythm
and depth. Suction airway hourly or as necessary to remove secretion. Administer prescribed inhalations or bronchodilators mucolytic as
ordered. Institute safety of the patient. Fall prevention. Side rails up low bed position. Prevent infection and potential complication. Provide patient and family education about treatment and
recovery of the patient.
NURSING INTERVENTION
Persons with ARDS are hospitalized and require treatment in an intensive care unit.
No specific therapy for ARDS exists. Supportive measures :
◦Supplemental oxygen ◦Mechanical respirator ◦Positioning strategies .
Medical management
–Fluid Administration – The patient should be
aggressively fluid resuscitated for any signs /symptoms of shock in order to optimize end organ perfusion. Once hemodynamic stability is achieved, fluid administration should be minimized to decrease the alveolar-capillary leak and pulmonary edema. Aggressive diuresis should also be considered once hemodynamic stability is achieved. Nutritional support should be initiated as early as possible.–
Fluid therapy
.Prone Positioning – Has been used since mid 1970’s in an effort to improve lung perfusion and oxygenation. Prone position or bed that provides continuous lateral position helps mobilize pulmonary secretions and improve ventilation/ perfusion matching. In prone position patient face down improves ventilation in posterior lung, where edema settles when patient in supine position . Risks are mainly logistical, i.e. dislodgement of endotracheal tube or vascular lines, increased intra-abdominal pressure, feeding intolerance, and edema (facial). The greatest effects are achieved when patients are maintained prone for 12 hours or longer and oxygenation improves in 60-70% of patients.
◦Antibiotics◦Anti-inflammatory drugs; such as corticosteroids
◦Diuretics◦Drugs to raise blood pressure◦Anti-anxiety◦Muscle relaxers◦Inhaled drugs (Bronchodilators)
MEDICATIONS
RECRUITMENT MANEUVER Patients with ARDS require support with mechanical
ventilator. Utilizing a CPAP mode and providing PEEP 35 to 40
for 40 second. In ventilator PEEP used to prevent alveolar de-
recruitment at end-expiration. In patients with ARDS, PEEP is used primarily to improve arterial oxygenation. Increased end-expiratory pressure increases mean airway and intra thoracic pressure. When applied correctly, this prevents alveolar collapse, increasing the volume of aerated lung by preventing alveolar de-recruitment at end-expiration
VENTILATOR SETTINGS
The beneficial effects of PEEP include improved total lung compliance, and decrease in the work of breathing for spontaneously breathing patients, and improved gas exchange through a reduction in intrapulmonary shunting and improved ventilation–perfusion matching. Improved gas exchange may allow for reduction in the fraction of inspired oxygen (FiO2) and oxygen toxicity. Furthermore, studies have suggested that PEEP can reduce the release of bioactive mediators by the lung and may reduce the incidence of secondary infections in the lungs
Common complications are;◦Nosocomial pneumonia: ◦Barotrauma◦Renal failure
Other complications are : ◦O2 toxicity, ◦stress ulcers, ◦Tracheal ulceration, ◦Blood clots leading to deep vein
thrombosis &◦pulmonary embolism.
COMPLICATION
Ineffective breathing pattern related to decreased lung compliance, decreased energy as characterized by dyspnea, abnormal ABGs, cyanosis & use of accessory muscles
Impaired gas exchange related to diffusion defect as characterized by hypoxia, & cyanosis.
Risk for decreased Cardiac output related to positive pressure ventilation.
Impaired physical mobility related to monitoring devices, mechanical ventilation & medications as characterized by imposed restrictions of movement, decreased muscle strength & limited range of motion.
NURSING DIAGNOSIS
Knowledge deficit related to health condition, new equipment & hospitalization as characterized by increased frequency of questions posed by patient and significant others & immobility.
Ineffective protection related to positive pressure ventilation, decreased pulmonary compliance & increased secretions as characterized by crepitus, altered chest excursion, abnormal ABGs & restlessness.
Risk for impaired skin integrity related to prolonged bed rest, prolonged intubation
ASSESSMENT NURSING DIAGNOSIS
PLANNING IMPLIMENTATION/RATIONALE
EVALUATION
Objective data: patient is dyspenic , restless, cyanosis and desaturated..
Impaired gas exchange related to diffusion defect as characterized by hypoxia, & cyanosis
After 12 hours of nursing intervention patient will shows signs of improved ventilation and adequate oxygenation.
Vital signs, breath sounds, breathing pattern and level of consciousness.Checked hourly.→Evaluated pulse oxymery.Shows 95%→Evaluated head of the bed 35 degree. →Suctioned secretion as needed →Administered bronchodilators, expectorance like syp:.mucolyte, as orders. →Blood gas analysis done 2 hourly .
→Evaluate the degree of compensation. →To evaluate o2 saturation. →Facilitate adequate oxygen intake →To clear the airway →To treat the underlying condition. →To check the gas level.
After 12 hours of nursing intervention patient exhibited signs of improved ventilation like free of distress, ABG shows Paco2 between 35-45.
Remain on modified bed restTake medication prescribed.Follow up regularly.Take adequate nutrition.Maintain personal hygiene.Maintain skin care.Regularly checkup vitals
. NURSING HEALTH TEACHING
This is the case of 25 years old male patient with the diagnosis of acute respiratory syndrome and septicemia. Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid resulting in severe dyspnea, hypoxemia and diffuse pulmonary infiltrates. Criteria which are fulfilled by the patient, conservative management rendered such as investigations , Antibiotics, Anti-inflammatory drugs; such as corticosteroids, Diuretics, Drugs to raise blood pressure, Anti-anxiety Muscle relaxers, Inhaled drugs (Bronchodilators).. A conservative fluid management strategy has been shown to reduce duration of mechanical ventilation andICU stay. Patient was intubated and on ventilator and fully sedated .patient developed hypotension and started inotropic support for two days. After all management patient was extubated and fully conscious and oriented. Patient shifted to surgery ward.
CONCLUSION
Wikipedia. Medical and surgical nursing book volume 1 and 2 of Brunner.
Luck man and Sorensen’s Medical-Surgical Nursing a Physiologic Approach 4th edition Lippincott Manual of Nursing Practice 9th edit.
BIBLIOGRAPHY