277Critical Care

PULMONARY

•   Complications related to pulmonary factors occur in 20% to 30% of postoperative patients. The functional residual capacity (FRC) is reduced when patients are supine, or have had a laparotomy. Vital capacity is decreased 45%, and FRC is reduced 20%.

•   Risk factors are: obesity, surgery longer than 2 hours, chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), renal failure, poor mental status, immunosuppression, nasogastric tube (NGT) use, narcotics, smoking, sleep apnea, and asthma. COPD patients can benefit from a preoperative arterial blood gas (ABG) and pulmonary function testing (PFT).

•   Correlation of operative time to complications has been reviewed and increased rates of: urinary tract infection (UTI), organ space surgical site infection (SSI), sepsis/septic shock, prolonged intubation, pneumonia, rate of deep vein thrombosis (DVT), deep incisional infection, and wound disruption were found. Per 1,000 cases, there were 116 occurrences per operating room hour (1).

•   Atelectasis usually occurs postintubation, and is due to surgical pain with its associated decreased inspiratory effort. Dyspnea, tachypnea, and fever can be present. Examination reveals crackles at the lung bases. Diagnosis is with chest x-ray (CXR). Treatment is incentive spirometry.

•   Pneumonia can present with dyspnea, tachypnea, fever, and decreased O₂ saturation. Examination reveals decreased breath sounds segmentally. Diagnosis is via CXR and documentation of infiltrate or consolidation. Treatment is with antibiotics, incentive spirometry, chest physiotherapy, and pulmonary toilet.

•   Respiratory failure is defined as altered pulmonary function that yields hypercarbia, acidemia, or hypoxemia.

        The etiology can be a decreased respiratory drive, airway obstruction, decreased pulmonary function, COPD, asthma, anaphylaxis, pulmonary edema from CHF, acute respiratory distress syndrome (ARDS), pneumonia, abscess, tuberculosis, pneumothorax, pleural effusion, hemothorax, cancer, anemia, or pulmonary embolus.

        Diagnosis is via physical examination, imaging, and laboratories. It is important to obtain a CXR, oxygen saturation monitor, an ABG, a complete blood count (CBC), electrolytes, a CT angiogram if suspicion for a pulmonary embolism (PE) is present, and potentially an echocardiogram (ECHO) to rule out cardiogenic etiology.

•   Oxygen is not as good as we think. 100% O₂ for greater than 6 hours has been shown to decrease macrophage activity, mucous velocity, cardiac output (CO), and can cause irreversible pulmonary damage if given for greater than 60 hours. Oxygen can be delivered via nasal prongs, a rebreathing face mask, a nonrebreathing face mask, continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), and intubation with mechanical ventilation. Delivery via nasal prongs has been shown to be as good as a rebreathing face mask.

•   Parameters

        PaO₂: arterial oxygen tension.

             Normal: 70 to 100 mmHg

        PaO₂: alveolar oxygen tension (FiO₂ × 713) − (PaCO₂/0.8).

             Normal: 100 mmHg

        PaCO₂: arterial CO₂ tension.

             Normal: 35 to 44 mmHg

        AA gradient: alveolar − arterial O₂ tension or [(FiO₂) × (Atmospheric pressure − H₂O Pressure) − (PaCO₂/0.8)] − PaO₂.

             Normal is 3 to 16 mmHg or (Age/4) + 4

        Vital capacity: volume of expired air after maximal inspiration.

             Normal: 3 to 5 L

        Tidal volume: volume of inspired air for each peak breath.

             Normal: 6 to 7 mL/kg

        FEV1: maximum volume forcefully expired in 1 second.

             Normal: greater than 83% of vital capacity

        PEF: peak expiratory flow rate.

             Normal: greater than 400 L/minute

        NIF: negative inspiratory force.

             Normal: 60 to 100 cm H₂O

•   Parameters for intubation in respiratory failure: indications for mechanical ventilation include hypoxemia, hypercarbia, respiratory acidosis, the inability to maintain or protect the airway including changes in mental status, and respiratory fatigue. The largest endotracheal tube possible should be chosen: this is usually a 7.5 to 8 for women. This is to decrease airway resistance. Vitals and laboratory benchmarks are listed below (Table 4.9).

•   The A-a gradient is calculated to determine shunt and help rule out a pulmonary embolus. The A-a gradient = [(FiO₂) × (Atmospheric pressure − H₂O pressure) − (PaCO₂/0.8)] − PaO₂. A normal gradient estimate = (Age/4) + 4.

•   Ventilation by machine can be run by volume or by pressure. The volume cycled setting has a preset tidal volume. The pressure cycled setting stops the cycle at a preset pressure; this setting is useful in hypoxic patients.

        Continuous mandatory ventilation (CMV) delivers a preset minute ventilation determined by a set respiratory rate and tidal volume. It is useful in heavily sedated patients, those given paralytic agents, and those who do not tolerate assisted ventilation.

        Assist–control (A/C or volume controlled) ventilation presets the tidal volume, and this tidal volume is delivered when a breath is initiated by the patient. This is the most common mode of mechanical ventilation used in the intensive care unit (ICU). A control back up rate is set to prevent hypoventilation.

        Intermittent mandatory ventilation (IMV) has a set rate and tidal volume, but allows unassisted spontaneous breaths and provides a full breath in relation to the amount of patient effort.

        Synchronized intermittent mandatory ventilation (SIMV) delivers breaths at regular intervals that are based on a preset tidal volume and rate which are synchronized with the patient’s respiratory efforts.

        Pressure supported (PS) ventilation provides constant airway pressure, which is delivered during inspiration. It is the most frequently used mode during “weaning.” In this mode, each time the patient inhales, the ventilator delivers a pressure-limited breath. The patient controls the rate, volume, and duration of the breaths.

•   To initially set the ventilator, IMV or A/C cycles are usually chosen. The FiO₂ is started at 60% (maximum), and weaned down to a patient O₂ saturation of 90% to 95% and a FiO₂ of 21% (room air [RA]). The rate is usually initiated at 8 to 12 breaths per minute. The tidal volume is chosen at 8 to 12 mL/kg, but should be lower at 6 mL/kg if the patient is suspected or diagnosed with ARDS. A positive end-expiratory pressure (PEEP) of 5 cm H₂O is also chosen. It is important to check an ABG and adjust the settings further based on those results.

•   Extubation should be a rapid goal. A spontaneous breathing trial or t-tube trial should be performed daily to assess patient status. Weaning settings on the ventilator are with SIMV or PS ventilation. To be extubated, the patient must be conscious and can protect the airway, the FiO₂ must be less than 50% (optimally at 21% RA), the PEEP should be less than 5 cm H₂O, the NIF should be greater than 20 cm H₂O (Table 4.10).

•   Ventilator acquired pneumonia (VAP) occurs in 30% of patients after 72 hours of intubation. The mortality of VAP is 25% to 50%.

•   Monitoring of pulmonary and cardiac status can be with a central line. The central venous pressure (CVP) is an assessment of volume status and crude cardiac function. It consists of multiple measurements, and is not a single number. A normal CVP is 8 to 10 cm H₂O, or 2 to 6 mmHg.

•   A pulmonary artery (PA or Swan) catheter can be helpful when it is important to know critical cardiac output (CO) or fluid status. Complications of a Swan include pneumothorax, arrhythmia, line sepsis (2%), or PA rupture. CO is calculated thermodynamically. An estimation of preload is obtained by wedging the end of the catheter into an afferent pulmonary capillary. This is called the pulmonary artery occlusion pressure (PAOP) or pulmonary capillary wedge pressure (PCWP). A normal PCWP is 6 to 12 mmHg. The PCWP is a crude reflection of the left arterial pressure. If the PCWP is elevated, then the preload is adequate or excessive; if it is low, then the patient is likely volume depleted. The mixed venous blood sample is blood obtained from the tip of the PA catheter and reflects the most desaturated blood in the body.

•   ARDS occurs after a defined insult to the lungs. This can include hemorrhage, sepsis, shock, or pneumonia. An ABG should be drawn.

        Symptoms are tachypnea, dyspnea, and respiratory failure.

        There are several criteria for the diagnosis of ARDS:

             Bilateral diffuse infiltrates are seen on CXR

             CHF and iatrogenic volume overload are ruled out by ECHO (showing an EF >35%)

             There is impaired oxygenation with documented oxygen saturation less than 92%

             The calculated PaO₂/FiO₂ is ≤ torr for the diagnosis of ARDS

             If the PaO₂/FiO₂ ≤ 300 torr, the diagnosis is acute lung injury (ALI)

        The mortality of ARDS is 30% to 40%.

        Treatment is with intubation, mechanical ventilation, antibiotics, and treatment of the underlying cause. Steroids have not been proven beneficial. Better survival has been seen with ventilatory support maintaining low tidal volumes to prevent barotrauma (6 mL/kg), and elevated PCO₂—permissive hypercapnia.

CARDIAC

•   Myocardial infarction can occur at any time during hospitalization. Any chest pain, arrhythmia, SOB, persistent dyspepsia, or arm pain should be worked up with cardiac enzymes and an EKG (serially) as well as a CXR to start.

•   Reinfarction can occur after a recent myocardial infarction (MI). Rates have decreased from 37% to now 5%-10% due to better medications used for reperfusion. The rate further decreases the longer the time from the initial insult. The rate is 2% to 3% after 4 to 6 months, and 1% to 2% if greater than 6 months have elapsed after a recent MI.

•   Perioperative prophylactic beta blockers have been studied. Laughton, in 2005, showed there were fewer infarctions and lower mortality when used after surgery. The rates of infarction with use were 24% versus 39% without. The 2-year mortality was 16% with use versus 32% without. A more recent study, the POISE study in 2008, refutes the benefit of beta blocker use postoperatively. There were fewer MIs in the beta blocker group (4.2% vs. 5.7%; p < 0.05), but there were more deaths (3.1% vs. 2.3%; p < 0.05) and more cerebrovascular accidents (1% vs. 0.5%; p < 0.05) with beta blocker use (2).

•   The role of a pulmonary artery catheter (Swan-Ganz) for surgery remains controversial and its use has decreased in modern clinical practice. There are no definitive studies that provide evidence of benefit in the surgical setting. The current indications are active CHF, severely depressed left ventricular (LV) function, and critical aortic stenosis.

•   Parameters

        CO: heart rate × Stroke volume.

             Normal: 4 to 8 L/min

        Cardiac index: CO/BSA m².

             Normal: 2.5 to 4 L/min

        MAP: mean arterial pressure = 1/3 × (SBP – DBP) + DBP.

             Normal: 70 to 105 mmHg

        PAP Systolic: systolic pulmonary arterial pressure.

             Normal: 15 to 30 mmHg

        PAP Diastolic: diastolic pulmonary arterial pressure.

             Normal: 5 to 12 mmHg

        PAP mean: mean pulmonary arterial pressure.

             Normal: 5 to 10 mmHg

        PAWP: pulmonary artery wedge pressure = LA and LV filling pressure.

             Normal: 5 to 12 mmHg

        SVR: systemic vascular resistance (MAP – MRAP) (80)/CO.

             Normal 900 to 1,400 dynes/sec/cm^-5

        PVR: pulmonary vascular resistance (mean PAP – PAWP)/CO.

             Normal 100 to 240 dynes/sec/cm^-5

        VO₂: O₂ consumption.

             Normal 115 to 1,165 mL/min/m²

        DO₂: O₂ delivery.

             Normal 640 to 1,000 mL O₂/min

•   Ischemic heart disease

        Ischemic heart disease (IHD) (MI) can often-times be identified by its symptoms. Angina, nausea, vomiting, dyspnea, sweating, diaphoresis, shortness of breath (SOB), weakness, anxiety, elevated blood pressure (BP), tachycardia, bradycardia, jugular venous distension (JVD), or tachyarrhythmias are often present.

        Workup includes: an electrocardiogram (EKG), cardiac enzymes × 3 q 6 to 8 hours (creatine kinase [CK], creatine kinase-MB [CKMB], troponin I), brain natriuretic peptide (BNP), CXR, and consideration of coronary angiography, especially if an ST elevation myocardial infarction (STEMI) is diagnosed.

        Medical treatment is with transfer to the critical care unit (CCU) for telemetry. MIs are classified as: STEMI, NSTEMI, and unstable angina. Pulse oximetry should be obtained, aspirin administered, and oxygen placed to keep saturations greater than 90%. A CXR should be obtained in addition to an EKG and laboratories. Initial stabilization should include administration of sublingual nitroglycerin (NTG) at 5 minute intervals for three doses if there is chest pain. IV morphine dosed at 4 to 8 mg repeated every 5 to 15 minutes is recommended for chest pain and to decrease the myocardial workload. Atropine can be given to increase blood pressure if hypotension is present due to bradycardia. Beta blockers should be administered in the absence of contraindications. Contraindications include: SBP less than 90, bradycardia, findings suggesting right ventricle infarction.

             Treatment of patients with STEMI include: IV thrombolysis within 30 minutes or cardiac catheterization with PTCA within 90 minutes of arrival or occurrence.

             Treatment of patients with NSTEMI include: observation and monitoring in a CCU with administration of stool softeners, stress ulcer prophylaxis, antipyretics, and bedrest. Beta blockers should be administered in the absence of contraindications. Angiotensin-converting enzyme (ACE) inhibitors may be additionally beneficial in limiting infarct size. If chest pain continues, angiography and revascularization via PTCA, stenting, or surgery is indicated. IV NTG titrated to 10 to 200 mg/min to prevent hypotension can be given to alleviate coronary artery spasm and decrease infarct size. Thrombolytic therapy is not indicated in NSTEMI myocardial infarction.

             Treatment of patients with unstable angina is angiography with PTCA, stenting, or surgery. An EKG should be obtained with each set of enzymes. An ECHO is usually ordered as well for ejection fraction and ventricular assessment. Angiography should be considered the timing of PTCA based on refractory or recurrent angina, new or evolving signs of CHF, hemodynamic instability, new arrhythmias, a temporal change in troponins, or a history of PTCA in the last 6 months. For severe LV dysfunction and cardiogenic shock, angioplasty, thrombolysis, and revascularization with multivessel stenting may be indicated.

        Interventional treatment:

             Angioplasty is used to dilate a stenosed artery mechanically with a balloon catheter.

             A stent can also be placed simultaneously. The stent can be mechanical alone or medicated (impregnated with paclitaxel). The medicated stents keep occluded arteries open and decrease local plaque. Noncardiac surgery can be performed 6 weeks after a medicated stent as antithrombotics are needed for this duration. A nonmedicated/bare metal stent is indicated if surgery is urgent. Surgery can be performed 2 weeks after bare metal stent placement.

             Thrombolysis is another option for removing coronary artery occlusion. This occurs after localization with angiography and if the diagnosis occurs within 6 hours of the onset of pain. The clot is lysed with antithrombotics.

•   Heart failure is defined as an EF less than 35% to 40%. The etiology is most commonly a MI, but can be viral or hereditary.

        Symptoms are SOB, lower extremity edema, or JVD. There can be ascites if there is significant right heart failure, progressing to anasarca if not managed.

        Workup includes a CXR, which will show bilateral infiltrates, an EKG, an ECHO, cardiac enzymes × 3 every 6 to 8 hours, BNP, electrolytes, and a CBC. A spiral CT can help rule out a PE.

         Treatment is with O₂ supplementation, water restriction to 2 L/day, morphine, and diuretics (furosemide to start at 20 mg IV, doubling of the dose is indicated if minimal response is seen). If there is a need to increase the CO, inotropes such as dopamine or dobutamine can be considered. Digoxin can be administered to improve contractility (1 mg load 0.5 mg IV, then 0.25 mg q6 hours × 2, maintenance 0.125 mg/day, checking the level the first day then every 5 days). A daily weight and strict salt management (<2 g/day) are important.

•   Pulmonary edema is characterized by SOB.

        Diagnosis is with a physical examination demonstrating bilateral rales and low oxygen saturation. Confirmation is with CXR showing bilateral infiltrates. An EKG, an ECHO, cardiac enzymes × 3 every 6 to 8 hours, BNP, an ABG, and CT angiogram to rule out PE should be obtained to rule out cardiac and venous thromboembolism (VTE) etiologies.

        Treatment is diuresis, O₂ supplementation, and correction of the underlying cause.

•   Hypertension (HTN) is often not symptomatic (Table 4.11).

        Characteristics when symptomatic are a headache or change in vision.

        Diagnosis is via BP assessment. If symptomatic, an EKG, cardiac enzymes × 3 every 6 to 8 hours, and CT head without contrast or MRI are indicated to rule out stroke.

        Parameters: grading of HTN is per Table 4.11.

        Treatment for crisis-range HTN can include: nitroprusside (Nipride) 1 to 10 mcg/kg/min IV; ACE inhibitor (enalapril) 12.5 mg PO or 1.25 to 2.5 mg IV every 6 hours; a beta blocker (labetalol) 20 mg IV, repeated at 40 to 80 mg q10 minutes with a maximum dose of 300 mg and a maintenance dose of 0.5 to 2 mg/min; an alpha blocker (hydralazine) dosed at 5 to 20 mg IV.

        Management of HTN, other than crisis range, is with single-agent or combination agents. First-line drugs are often diuretics (hydrochlorothiazide). Beta-blockers can be first- or second-line, as can be calcium channel blockers (a better response is seen with these drugs in African Americans). ACE inhibitors and angiotensin receptor blockers (ARBs) can be used if there are contraindications to other medications, or they can be used in combination.

•   Arrhythmias are abnormal rhythms of the heart rate. It is important to always rule out a MI. If the patient is unstable, cardioversion should always be performed. Secondary investigation is directed at abnormal electrolytes, endocrine issues (thyroid-stimulating hormone [TSH]), and drug toxicity. Most arrhythmias are transient.

         Atrial fibrillation is a tachyarrhythmia. Diagnosis is via EKG, which shows an irregularly irregular rhythm with no P wave. Treatment is with IV diltiazem. A beta blocker can be helpful if there is a rapid ventricular response. Amiodarone has a lower incidence of recurrent atrial fibrillation. Digoxin can also be used if low blood pressure accompanies the arrhythmia. If there is persistent atrial fibrillation, chronic anticoagulation should be considered based on the CHADS₂ score. The CHADS₂ score is based on patient risk factors. These include: HTN greater than 140/90; age greater than 75; diabetes mellitus (DM); history of CVA or TIA; or history of VTE. All risk factors are given a score of 1 except for the CVA and VTE components which are scored at 2 each. If the score is a 2, warfarin is recommended (Table 4.12).

        Atrial flutter is a tachyarrhythmia. Diagnosis is via EKG, which shows a saw tooth pattern. Aspirin (ASA) prophylaxis is indicated.

        Supraventricular tachycardia is a tachyarrhythmia. Diagnosis is via EKG, which shows tachycardia with no P waves. Treatment is initiated with vagal maneuvers. If this is unsuccessful, adenosine can be administered up to three times (given IV at 6 mg, again at 6 mg, then at 12 mg if no initial response).

        Bradycardia is defined as a pulse less than 60 bpm. Diagnosis is via EKG. If the patient is symptomatic and not stable, the patient should be paced transcutaneously until a permanent pacemaker can be placed or the etiology diagnosed. If the patient is stable, treatment is with atropine dosed at 1 mg IV.

        Postoperative atrial fibrillation after noncardiac surgery: the differential diagnosis includes: hypovolemia, intraoperative hypotension, trauma, pain, acute anemia, hypoxia, hypokalemia, low magnesium, hypervolemia or MI. A goal is HR 80 to 100 bpm, not rhythm control. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial was the largest trial to compare rate with rhythm control; 73% versus 80.1% (NS) of adverse events were observed in the rhythm control arm. Management pathways are determined by symptoms (3).

             Symptomatic (unstable BP, pulmonary edema, chest pain, change in level of consciousness): direct cardioversion. If the patient declines, then IV metoprolol, IV diltiazem, IV amiodarone, or IV digoxin should be administered.

             Asymptomatic: determine the ejection fraction (EF) (order ECHO). Consider direct current cardioversion (DCC). If the EF is:

                  Greater than 45%: then oral metoprolol, diltiazem, amiodarone, digoxin.

                  Less than 45%: consider oral medications, or IV diltiazem, IV amiodarone, or IV digoxin. Flecainide and propafenone can be used if duration less than 7 days. Amiodarone, dofetilide, or ibutilide should be used if there are cardiac comorbidities.

             It is important to restart beta blockers or calcium channel blockers that were used as maintenance preoperatively.

             If atrial fibrillation persists greater than 48 hours, the need for chronic anticoagulation should be assessed.

             Risk scoring system: CHA2DS2VASc scoring system. A score ≥2 is high risk and oral anticoagulation is indicated.

             Postoperative patients have a high risk of hemorrhage with anticoagulation: the HAS-BLED surgical scoring system risk assesses for hemorrhage. A score ≥3 indicates high risk of bleeding: some versions include alcohol use and antiplatelet medications for one point each (4).

SHOCK AND SEPSIS

•   Shock is defined as a decrease in tissue perfusion. There are five types of shock: septic, cardiogenic, hemorrhagic, neurogenic, and iatrogenic. Diagnosis is via physical examination, vitals, EKG, and lab tests. Treatment generally consists of intravenous fluid (IVF) and type-directed support.

        Cardiogenic shock can be due to MI, HTN yielding a heavy afterload and severe cardiac strain, or pump failure from too much volume. Cardiogenic shock is managed by diuretics to reduce the preload, dopamine or dobutamine to increase cardiac function, norepinephrine if dopamine fails, and nitroprusside or a nitroglycerine drip for venous capacitance. Angiography with angioplasty, stent placement, left ventricular assist device (LVAD), or coronary artery bypass grafting (CABG) surgery can be employed for acute management.

         Hemorrhagic shock is managed by IVF replacement (3:1 ratio of IVF to blood loss) and blood products, surgery for hemostasis, or embolization.

        Neurogenic shock often occurs from embolic or hemorrhagic stroke, head trauma, or metastatic disease. It is managed by IVF, pressor support, hyperventilation with intubation if necessary, XRT with steroids to reduce local inflammation, and potential surgery if a mass effect is present.

        Iatrogenic shock is usually related to anaphylaxis. Treatment is to stop the offending medication/infusion, administration of steroids, antihistamines, O₂, and pressor support as indicated.

        Septic shock, see the following.

•   Generally, the systemic inflammatory response syndrome (SIRS) occurs when two or more of the following are documented in the setting of a known cause of inflammation: a body temperature greater than 38°C or less than 36°C; a pulse greater than 90 bpm; a respiratory rate greater than 20 bpm or a PaCO₂ ≤ 32; a WBC greater than 12 × 10³/mcL, or less than 4 × 10³/mcL, or greater than 10% band forms. In 2001, additional criteria were added for an inclusive approach to SIRS. These include: an altered mental status, oliguria, skin mottling, coagulopathy, hypoxemia, and hyperglycemia without a diagnosis of diabetes, thrombocytopenia, and altered liver function tests (LFTs).

•   A high level of suspicion should be maintained for SIRS with suspicion of organ dysfunction determined by:

        Decreased perfusion: capillary refill greater than 3 seconds, skin mottling, cold extremities.

        Lactate greater than 2 mmol/L.

        Circulatory: SBP less than 90 mmHg, MAP less than 65 mmHg, decrease in SBP greater than 40 mmHg.

        Respiratory: PaO₂/FiO₂ less than 300; PaO₂ less than 70 mmHg; SaO₂ less than 90%.

        Hepatic: jaundice; total bilirubin greater than 4 mg/dL; increased LFT’s; increased PT.

        Renal: creatinine greater than 0.3 mg/dL; urine output less than 0.5 mL/kg/hr for at least 2 hours.

        Central nervous system: altered consciousness, confusion, psychosis.

        Coagulopathy: international normalized ratio (INR) greater than 1.5 or a partial thromboplastin time (PTT) greater than 60 seconds, thrombocytopenia (platelets less than 100,000/mm³).

        Splanchnic circulation: absent bowel sounds.

•   Sepsis (septic shock) is SIRS due to a known infection. Septic shock is sepsis with hypotension despite adequate fluid resuscitation. There are two stages: early hyperdynamic and late hypodynamic. The crude mortality is 28% to 50%. 3 and 6 hour time marks are used to mark and respond to interventions.

•   The SOFA (sequential organ failure assessment) score is an assessment tool to determine extent of organ dysfunction. An increase in the SOFA score during the first 24 to 48 hours in the ICU predicts a mortality rate of at least 50%, up to 95%. Scores less than 9 predict mortality of 33%, and those above 11 can be predictive of mortality above 95%. The total points are tallied for the final score. The worst score in the past 24 hours is used to calculate the total score.

287•   Respiratory system

•   Nervous system

•   Cardiovascular system

•   Liver

•   Coagulation

288•   Kidneys

The Quick SOFA tool can identify patients at risk of sepsis: the presence of two or more qSOFA criteria points, of a total of three, represents organ dysfunction.

        Altered mental status with Glasgow Coma Score less than 15.

        Respiratory rate ≥ to 22 breaths/min.

        Systolic BP ≤ 100 mmHg.

             Intervention is needed with transfer or admit to the ICU.

                  Lines: an arterial line is needed to measure the MAP; consideration of a PA catheter for measurement of the CO, a Foley catheter to measure urine output.

                  Laboratories: an ABG to measure the PaCO₂ and PaO₂; CBC, serum lactate (≥2 mmol/L) or POC lactate, coagulation profile, d-dimer, fibrinogen, LFTs, total bilirubin, albumin, comprehensive metabolic panel (CMP), magnesium, phosphorus, calcium, 1,3 beta-D-glucan assay, mannan and antimannan antibody assays if candidiasis is in the differential diagnosis.

                  Cultures for: bacteria, fungus, and virus. These should be obtained from blood, urine, sputum, and wound before antimicrobial therapy is initiated. A delay of ≥45 minutes is considered substandard for antibiotic initiation. At least two sets of blood cultures (aerobic and anaerobic) with at least one drawn percutaneously and one drawn through each vascular access devices, unless it was inserted less than 48 hours prior, are necessary.

                  Imaging should be performed to rule out site of infection.

             Goals: a CVP of 8 to 12; a MAP ≥65, CVP 8 to 12 mmHg (12–15 if intubated) a urine output ≥0.5 mL/kg/hr; a ScvO₂ ≥70% or a mixed venous oxygen saturation ≥65%, and a normalized lactate level if initially elevated. Goals are desired within 6 hours. If oxygen saturation goals are not met in 6 hours, it may be beneficial to transfuse packed red blood cells (PRBC) to achieve a hemoglobin greater than 10 g/dL.

             Management:

                  Antimicrobial therapy: administration of broad spectrum IV antimicrobials within the first hour of recognition of septic shock and severe sepsis without septic shock is indicated. This should include one or more drugs that have activity against all likely pathogens to include bacterial and/or fungal and/or viral. Low procalcitonin levels can assist the clinician in the discontinuation of empiric antibiotics in patients who initially appeared septic, but have no laboratory evidence of infection. Combination empirical antimicrobial therapy should be started for neutropenic patients with severe sepsis. Empiric combination therapy should not be administered for more than 3 to 5 days. Antimicrobial regimen should be reassessed daily for potential de-escalation to the most appropriate single therapy as soon as the susceptibility profile is known. Duration of therapy is typically 10 to 14 days after negative blood cultures. Longer courses may be appropriate in patients who have a slow clinical response, undrainable foci of infection, bacteremia with Staphylococcus aureus, some fungal and viral infections, or immunologic deficiencies, including neutropenia. Antiviral therapy should be initiated as early as possible in patients with severe sepsis or septic shock of viral origin. For patients with difficult-to-treat, multidrug-resistant bacterial pathogens:

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