8/1/2016 ICU CONDITIONS S. Lawler Deep vein thrombosis • Patients requiring intensive care are at risk for the development of deep venous thrombosis and pulmonary embolism (PE). • Risk factors include immobility, venous stasis, poor circulation, major surgery, malignancy and pre-existing illness. • Over and above these well-known factors, intensive care itself is an independent risk factor (sedation and ventilation) 1 8/1/2016 • in critically ill patients, 95% of DVTs are clinically silent • ICU patients may require mechanical or chemical prophylaxis depending on risk factors for bleeding Pulmonary embolism • Pulmonary thromboembolism is common in immobile, critically ill, traumatised and postoperative patients. • The effects range from mild discomfort and shortness of breath to sudden profound collapse and cardiac arrest. 2 8/1/2016 Management • Oxygenation : high inspired oxygen; intubate/ventilate as necessary. • Optimisation of cardiovascular status • Major embolism: thrombolysis, e.g. streptokinase • For smaller embolism- anticoagulation, eg heparin infusion Shock • The primary function of the cardiovascular system is to maintain the perfusion of organs and tissues with oxygenated blood. • When these mechanisms fail, ‘shock’ ensues, which, if uncorrected can result in organ failure, prolonged ICU stay and death. 3 8/1/2016 Shock • Definition: • Shock is a syndrome of cardiovascular system failure resulting in inadequate tissue perfusion. • Hypotension is a common but not universal feature. Types • Cardiogenic- impaired left ventricular function leads to decrease in stroke volume, low blood pressure and inadequate tissue perfusion this results in a sympathetic response of vasoconstriction and increased SVR so patients peripheries will be cool, and urine output will be poor. • Hypovolaemic- blood/blood/plasma loss from an organ or tissue injury. Decreased intravascular volume,decreased venous return decreased stroke volume/CO/BP/TP 4 8/1/2016 • Septic- Severe sepsis in the presence of hypotension unexplained by cardiovascular insufficiency.causes are organisims such as Klebsiella;enterobacter, E.Coli and opportunistic fungi • An immune response is triggered releasing macrophages monocytes and neutrophils that interact with the vascular endolthelial cells, releasing chemicals and toxins resulting in microvascular injury vasodilation of capillary bed ,capillary leak tissue ischaemia decreased circulating volume and decreased oxygen delivery and consumption Classification Underlying cause Hypovolaemia Dehydration Haemorrhage Burns Sepsis Cardiogenic Mycocardial infarction/ischaemia Valve disruption Mycocardial rupture (e.g. VSD) Altered systemic vascular resistance Sepsis Anaemia Anaphylaxis 5 8/1/2016 Clinical features • The clinical features vary depending on the cause and the physiological response. Two patterns are typically recognised, although there is a continuum from one to the other: Warm pink vasodilated, hyperdynamic patient with high cardiac output and hypotension. Cold, grey, sweaty, vasoconsricted, peripherally shut down patient with low cardiac output. Blood pressure may be maintained in the early stages. Features Other features of shock may include increased or decreased core temperature, hypoventilation or hyperventilation, renal and hepatic dysfunction, disseminated intravascular coagulation, and altered mental status (Rapid shallow breathing, decreased urine output, confusion, tachycardia, profound hypotension, cold clammy skin) 6 8/1/2016 Management Optimisation/restoration of oxygen deliveryoxygen therapy Optimisation of cardiac output-intravenous fluid administration and RBC transfusion Optimisation of blood pressure- Vasoactive agents and ionotropes Renal dysfunction • Renal dysfunction is common in the ICU and frequently occurs as part of a syndrome of multiple organ failure. • It is usually manifest as oliguria progressing to anuria, but highoutput renal failure, in which there are large volumes of poorly concentrated urine, may also occur. 7 8/1/2016 • The mortality rate for patients in intensive care who develop ARF is increased to around 50%. • The high mortality rate probably reflects the seriousness of the underlying condition, rather than mortality specifically attributable to renal failure. • Patients usually die with renal failure rather than from renal failure. • Classically, the causes of acute renal dysfunction are divided into prerenal (inadequate perfusion), renal (intrinsic renal diseaseproblem is with kidney tissue itself) and postrenal (obstruction to urine out flow). 8 8/1/2016 Cardiac failure Heart failure is common and represents an inability of the heart to maintain sufficient CO despite adequate filling. The clinical picture may range from mild peripheral oedema and shortness of breath to florid pulmonary oedema and hypotension. The principles of management: Oxygenation CPAP by face mask / non-invasive ventilation. Invasive monitoring as necessary- Arterial line, central venous or pulmonary artery catheter. inotropes if required. Infection May be primary cause of admission or icu aquired Increased risk of cross infection Immune suppressive effects of drugs Poor nutrition and impaired tissue healing Effects of sedative agents and analgesia eg.suppressed cough reflex, gi stasis ETT Vascular catheters, urinary catheters and drains 9 8/1/2016 Typical signs of infection in critically ill Pyrexia Tachycardia Hyperventilation (failure to wean) Raise in WCC Non-specific deterioration in condition Systemic inflammatory response syndrome (Van Aswegen and Morrow,2015) • SIRS is a systemic inflammatory response to overwhelming clinical pathologies such as burns, trauma, ischaemia and inflammation whereas sepsis is a systemic response to infection. • Criteria for diagnosing SIRS and Sepsis Temperature >38* or <36* HR >90 beats per min Resp rate > 20 breaths/per min or PaC02< 32mmHg White blood cell count > 12000 or < 4000 2 or more of the above after severe clinical insults= SIRS 2 or more of above in presence of infection =sepsis 10 8/1/2016 • During SIRS or SEPSIS an increase in circulating cytokines result in tissue damage and dysfunction of vital organs. • Pro inflammatory Cytokines cause a breakdown in muscle protein and reduction in muscle mass leading to muscle weakness. Disseminated intravascular coagulopathy • Arises from generalised activation of the inflammatory cascade often following septic shock, burns, lung contusion • It involves clotting within the vasculature(fibrin and platelets) resulting in tissue damage • Normal clotting fails to take place because of depletion of clotting factors • This will give rise to bleeding from the slightest trauma eg. suction • Nasopharyngeal suction is contra indicated • Ett suctioning very cautiously 11 8/1/2016 Multiple organ dysfunction syndrome(MODS) • Presence of a systemic inflammatory response (e.g. SIRS criteria) and dysfunction of at least 2 organs • may be mild, or severe resulting in death • organ dysfunction may present as: • • • • • • • Acute kidney injury ARDS Cardiomyopathy Encephalopathy GI dysfunction Hepatic dysfunction Coagulopathy and bone marrow suppression 12 8/1/2016 ICUAW • Intensive care unit–acquired weakness, develops in individuals who are admitted to the intensive care unit for any reasons, commonly including sepsis and ARDS. • Many of these conditions require interventions that may limit patients mobility and therefore their function eg. MV, haemodialysis, ionotropes etc • Intensive care unit–acquired weakness is a specific term describing diffuse, symmetrical, widespread muscle weakness that develops after the onset of critical illness without other recognisable causes. • It is associated with increased rates of morbidity and mortality as it results in respiratory muscle weakness- prolonged ventilation, increase in the length of ICU stay and therefore increased risk for secondary complications (El Said, 2014) • Muscle weakness acquired in the ICU contributes to impaired physical function and is a common and major long-term complication in patients with critical illness often seen up to five years post discharge (Nordon-craft et al, 2011) 13 8/1/2016 • ICUAW may develop if an individual is on mechanical ventilation for as little as 4 to 7 days • Approximately 46% of the patients with severe sepsis, multiple organ failure, or prolonged mechanical ventilation will develop ICUAW (Appleton and Kinsella, 2012) • Complications of bed rest in patients with critical illness include systemic inflammation, atelectasis, metabolic and microvascular dysfunction, joint contractures, skin ulcers, and muscle weakness. • During bed rest, patients do not receive the beneficial effects of exercise, which reduces systemic inflammation. • In patients with critical illness and on bed rest, the loss of lean body mass in patients has been shown to be approximately 1% per day, or 7% per week. 14 8/1/2016 • Patients with ICUAW are often identified either due to difficulty to wean from ventilation or if the patient displays severe weakness having unexpected difficulty mobililising • In order to properly examine the patient physically the patients co-operation and maximal effort has to be attained. • This is not always possible as ICU patients are sedated and delirious with reduced cortical brain function. • ICUAW is diagnosed in awake and cooperative patients by bedside manual muscle testing using the Medical Research Council sum score Probable Risk factors for ICUAW (Kress and Hall,2014) • Severe sepsis/septic shock • Multiorgan failure / Increasing duration of multiorgan failure • Prolonged mechanical ventilation/bed rest • Increasing duration of SIRS • Hyperglycaemia-by inducing neural mitochondial dysfunction (Kress and Hall,2014) • Glucocorticoid and NMBA use • Female sex 15 8/1/2016 • ICUAW may be classified as critical illness myopathy (CIM), • critical illness polyneuropathy (CIP), • or a combination of both referred to as critical illness polyneuromyopathy (CIPNM or CINM). Signs • Symmetrical flaccid weakness of the limbs more pronounced in proximal rather than distal muscles. • CIP and CIM have similar presentations which cannot be reliably differentiated clinically. • The earliest sign may be facial grimacing in response to painful stimuli without limb movement • Muscle wasting is frequently disguised by oedema • The MRC sum score is used to assess muscle power in the awake patient. • A score less than 48 out of 60 indicates ICUAW-but cannot differentiate between CIM and CIP • Thereafter EMG and nerve conduction studies may be conducted to determine compound motor action potentials and sensory nerve action potentials • Hand dynamometry and grip strength has also been used as an outcome measure to detect icuaw 16 8/1/2016 CIP People with CIP have impairments of the neuromuscular system, including weakness, reduced deep tendon reflexes, and impaired pain, temperature, and vibratory sense. Cranial nerves typically are spared; however, facial weakness can occur. Weakness typically occurs in a symmetric pattern in the shoulder and hip girdles weakness can include the respiratory muscles making weaning from mechanical ventilation very difficult 17 8/1/2016 CIM Individuals with CIM display extreme weakness, particularly of proximal muscles. Deep tendon reflexes may be preserved or diminished. However, in contrast to CIP, sensation is intact. The MRC scoring system is used to determine muscle strength Evaluation of the level of patient cooperation Five standard questions Open and close your eyes Look at me Open your mouth and put your tongue out Nod your head Raise your eyebrows after I have counted to five Each correct answer is worth 1 point A score of 5/5 is required to assess volition muscle strength 18 8/1/2016 Medical Research Council Scoring System13. Amy Nordon-Craft et al. PHYS THER 2012;92:1494-1506 © 2012 American Physical Therapy Association Criteria for diagnosing ICUAW are the presence of 1, 2, 5, and either 3 or 4 (Appleton and Kinsella, 2012) 1. Weakness developing after the onset of critical illness 2. The weakness being generalized (involving both proximal and distal muscles), symmetrical, flaccid, and generally sparing the cranial nerves (e.g. facial grimace is intact) 3. Muscle power assessed by the Medical Research Council (MRC) sum score of less than 48 (or a mean score of less than 4 in all testable muscle groups) noted on more than 2 occasions separated by more than 24 hrs 4. Dependence on mechanical ventilation 5. Causes of weakness not related to the underlying critical illness excluded 19 8/1/2016 • Patients with persistent coma after sedation should undergo cns studies eg cranial ct scan and mri • If studies are normal electrophysiological studies/muscle biopsies should be performed (Kress and Hall,2014) Diagnostic algorithm • Please refer to article entitled “ICU-Acquired Weakness and Recovery from Critical Illness” John P. Kress, and Jesse B. Hall (N Engl J Med 2014;370:162635) 20 8/1/2016 Management • Prevention- the aims are aggressive treatment of sepsis, early mobilization, preventing hyperglycemia with insulin- tight glyceamic control to reduce catabolic syndrome • Minimising the use of corticosteroids and neuromuscular blocking agents even though evidence for this is scarce • Rehabilitation- prolonged bedrest is harmful contributing to skin ulceration, compression neuropathies, DVTs, and reduced muscle size, strength, co-ordination, balance, endurance function and low mood -deconditioning (Appleton and Kinsella,2012). • Passive and active movements as well as sitting up in bed/EOB sit to stand and standing must commence in the ICU. Prevention rehab (Hermans &Van den Berghe, 2015) • This method is aimed at reducing immobilisation • Sedation levels have to be decreased to the minimal level needed for safety or comfort • Passive/active movements using a bedside ergometer • 20 mins of bed-cycling 5 times per week from day 5 following icu admission- this training improved quads strength at hospital d/c and HRQoL in patients receiving this regime as opposed to conventional therapy. • Another approach used early mobs and OT within 72 hours of initiation of MV. • training consisted of individual programmes of PROM – AROM-bed mobs-sitting-t/f training then walking results showed that early mobs prevented ICUAW 21 8/1/2016 ELECTRICAL MUSCLE STIMULATION • A significant number of ICU patients are not able to participate in early mobs • EMS has been used in this population to preserve some muscle function during this phase however evidence for this approach remains inconclusive (Hermans &Van den Berghe, 2015). • EMS in conjunction with active exercises for a group of pts with copd on Mv was found to be more beneficial than the exercise only group. They demonstrated greater strength gains and were able to do bed to chair t/f earlier. • Cycle ergometry for unresponsive patients has also been found to be greatly beneficial demonstrating greater quads strength and greater distances in six min walk test (Nordon-craft et al,2012) Criteria for Beginning Physical Rehabilitation • Sufficient evidence is available to recommend safe physical rehabilitation for individuals with ICU-acquired weakness. • Rehab may begin as soon as the patients have sufficient medical stability to cope with the increased vascular and oxygen demands that accompany the physical examination and intervention • Decisions to mobilise or stop treatment requires careful interpretation of the patients presentation per encounter in order to ensure that the patient is physiologically capable to tolerate the rehabilitation • An algorithim checklist for mobilisation is below 22 8/1/2016 Criteria for mobilisation (Nordon-Craft et al , 2012) Physical therapy intervention techniques (Nordon-Craft et al , 2012) 23 8/1/2016 Principles of prescription Recommendations Exercise Prescription Frequency Start with once a day and progress Intensity Aerobic:40-70% of Max HR/11-13 on the Borg scale Resistance exercises: Start with 45%-50% of 1RM rogress to 50-70% 1RM Rest 1-2 mins between exercises Type Aerobic exercises: bedside ergometer; walking; step climbing;treadmill, walking running; stationery bike Resistance exercises-body weight, freeweights,resistance bands,weight machines Concentric, eccentric and isometric exercises of the trunk, upper and lower limbs.Uni and bilateral limb exercises Single and mulitiple joint exercises Time Aerobic:start with 5-10mins and progress to 20 mins These recommendations are for patients in the acute and subacute phases of recovery post traumatic surgery (van Aswegen and Morrow;2015) 24 8/1/2016 Considerations • One of the most difficult decisions to make when managing these patients is how far to push them. precise clinical guidelines do not really exist and the approach requires good clinical reasoning and interpretation of changes Cessation of treatment can be decided on haemodynamic instability and/or decreasing pulmonary status Some literature recommends initiating treatment with the least challenging to most challenging activities, while other literature suggest the opposite in order for the patient to practice the most functionally relevant tasks (Nordon-Craft et al , 2012). Dosage (intensity,duration,frequency) for exercise ranges from fifteen minutes to one hour 1-2 times per day, 5-7 days per week A team approach is absolutely necessary for the successful mx of these patients. Prognosis • Impairments of the respiratory, renal and CVS systems generally resolve however neuromuscular impairments take much longer and resolution is often incomplete • Survivors frequently report fatigue, weakness and cognitive changes including impaired functional ability up to a year post d/c. Activity limitations can persist for up to years post d/c (Nordon-Craft et al,2012) • ICUAW has been found to be an independent threat for prolonged ventilation increased length of ICU stay and increased mortality even post discharge at one year (Hermans and Van der Berge,2015) • Approximately 45% of patients with this condition will die in hospital and a further 20 % in the first year post discharge . Complete functional recovery only appears in 68% of patients (Appeleton,2012) 25