La precarización laboral: un reto multidimensional

Greenwich Medical Media, 2002.

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One requirement for continuous renal replacement therapy (CRRT) including haemofiltration is the need for anticoagulation. This may increase the likelihood for bleeding in the patient. However, in the absence of effective anticoagulation, this may result in clotting of the filter and inefficient renal replacement therapy. Blood flow, dialyser type, coagulation pathway activation, and convective mass transfer are among the factors which may increase the risk of clotting problems. Heparins are widely used for anticoagulation, but due to their potential side effects such as bleeding and heparin-induced thrombocytopaenia, alternative anticoagulation protocols should be considered. These include citrate anticoagulation, regional heparin/protamine, pre-dilution, and prostacyclin. Regional citrate use in the extracorporeal circuit provides anticoagulation by chelating calcium, and calcium is necessary for blood coagulation. This effect is reversed by calcium infusion into the systemic circulation. Citrate metabolism in liver and skeletal muscle generates bicarbonate. Hypernatraemia, metabolic alkalosis, hypocalcaemia, and hypercalcaemia are potential complications of this anticoagulation method.

Increasing the proportion of replacement fluid delivered pre-filter (predilution) will decrease the viscosity of blood in the circuit and decrease clotting risk at the expense of less efficient clearance of solutes. Drugs such as prostacyclin (epoprostenol) that inhibit interaction between platelets and artificial membranes were introduced as an alternative anticoagulant strategy for CRRT.

1. Schetz, M. Anticoagulation for continuous renal replacement therapy. Curr Opin Anaesthesiol 2001; 14: 143-9.

2. http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20 Guideline.pdf (accessed 12th September 2014).

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The oesophageal Doppler cardiac output monitor uses the Doppler principle to measure the velocity time integral for blood flow in the descending aorta. Coupled to an estimation of aortic root cross-sectional area and mathematical modelling, these data can produce estimates of stroke volume and cardiac output via a minimally invasive means. Oesophageal Doppler monitoring works under two key assumptions. Firstly, that derivation of aortic cross-sectional area is estimated — this is usually via a specific nomogram. Secondly, that a constant percentage of the cardiac output enters the descending aorta, as measurements with the probe clearly exclude coronary and cerebral circulations. As such, a correction factor must be applied to the readings to give true cardiac output.

Peak velocity is an age-dependent measure of contractility, independent of afterload. The flow time (FT) is dependent on heart rate, and as such is usually corrected using a derivation of Bazett’s formula to a rate of 60bpm (1 second per cardiac cycle). As such, systolic flow time should be roughly a third of this and so a normal FTc has a range of 330 to 360 milliseconds. A high FTc usually reflects a reduction in afterload such that the systolic time promotes extended flow. This can be seen in vasoplegia from sepsis and drug administration, but should be balanced against the shortening of the FTc that can be seen with either preload reduction or occasionally, myocardial depression.

There are multiple relative contraindications to insertion, including nasal trauma, oesophageal varices, surgery, stent or carcinoma, and intra-aortic balloon pump placement. While the probe is commonly placed via the nasal route, it can be passed orally into the oesophagus in cases of nasal injury or suspected base of skull fracture.

1. King SL, Lim MS. The use of the oesophageal Doppler monitor in the intensive care unit. Crit Care Resusc 2004; 6: 113-22.

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A creatinine clearance of 30-59ml/min denotes moderate renal impairment (chronic kidney disease stage 3). Many renally excreted drugs need dose adjustment to prevent accumulation of the drug with potentially serious side effects (Table 2.1).

1. Ashley C, Currie A, Eds. The Renal Drug Handbook, 3rd ed. London, UK: Radcliffe Publishing, 2004.

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About 20-25% (range 17-40%) of the 150,000 ischaemic strokes in the United Kingdom each year affect posterior circulation brain structures (including the brainstem, cerebellum, midbrain, thalamus, and areas of

Table 2.1.

Examples of dose adjustments for common antimicrobials in the presence of renal impairment. Drug Amphotericin B lipid preparation Clarithromycin Meropenem Metronidazole Tazocin Route IV IV/PO IV IV PO IV Normal dosing schedule 3-5mg/kg Q24h 500mg Q12h 1-2g Q8h 500mg Q8h 400mg Q8h 4.5g Q8h-Q6h Moderate renal impairment CrCl 30­59ml/min No change No change 1-2g bd No change No change No change Severe renal impairment CrCl 10­29ml/min No change No change 1g bd or 500mg tds No change No change CrCl 10-20ml/min 4.5g Q12h

Very severe renal impairment CrCl <10ml/min No change No change 1-2g od No change No change 4.5g Q12h

temporal and occipital cortex), which are supplied by the vertebrobasilar arterial system and therefore not assessed by routine carotid Doppler assessment. Early recognition of posterior circulation stroke or transient ischaemic attack (TIA) may prevent disability and save lives; however, it remains more difficult to recognise and treat effectively than other stroke types. Delayed or incorrect diagnosis may have devastating consequences, including potentially preventable death or severe disability. Preceding posterior circulation TIA or other transient brainstem symptoms, particularly if recurrent, signal a high risk of impending ischaemic stroke and should prompt urgent specialist referral. Such posterior circulation strokes may lead to oedema and swelling in areas of the brain with limited capacity for expansion, thus leading to the need for neurosurgical decompression procedures. The risk of recurrent stroke after posterior circulation stroke is at least as high as for anterior circulation stroke, and vertebrobasilar stenosis increases the risk three-fold.

1. Merwick Á, Werring D. Posterior circulation ischaemic stroke. Br Med J 2014; 348: g3175.

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The intra-aortic balloon pump (IABP) is one of the most widely used circulatory assist devices for critically ill patients. Although supporting evidence is limited, it remains a regularly utilised therapy and as such the practising intensivist must understand the principles and rationale for insertion. The primary role of the IABP is to increase myocardial oxygen supply and thus facilitate an improvement in ventricular performance. It achieves this by inflating at the onset of diastole, timed with the dichrotic notch, to increase coronary perfusion pressure prior to the next systolic contraction. The balloon deflates just before systole, thus reducing afterload and further improving cardiac performance. Proposed indications for insertion include acute myocardial infarction, cardiogenic shock, ventricular failure and cardiac surgery.

Helium is used to inflate the balloon to provide rapid gas transfer via laminar flow and to allow absorption within the bloodstream in the unlikely

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event of balloon rupture. The balloon is positioned 2-3cm distal to the origin of the left subclavian artery.

Trial data supporting use are weak. A systematic review has suggested insufficient evidence to support incorporation to guidelines. In 2012, the further results of IABP Shock II suggested no difference in mortality for patients with acute myocardial infarction complicated by cardiogenic shock randomised to IABP or conservative management.

1. Krishna M, Zacharowski K. Principles of intra-aortic balloon pump counterpulsation. Contin Educ Anaesth Crit Care Pain 2009; 9(1): 24-8.

2. Sjauw KD, Engström AE, Vis MM, et al. A systematic review and meta-analysis of intra- aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? Eur Heart J 2009; 30(4): 459-68.

3. Thiele H, Zeymer U, Neumann FJ, et al. Intra-aortic balloon support for myocardial infarction with cardiogenic shock New Engl J Med 2012; 367(14): 1287-96.

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pH, PCO₂and PO₂are direct measurements and HCO₃-_{, base excess}

and oxygen saturations are derived measurements. The electrodes in the blood gas analyser are maintained within narrow limits (37+/- 0.1°C) and the blood sample is warmed to this value before it is analysed. pH, and PCO₂ and PO₂ change with a change in temperature. Blood gas machines can calculate a pH, PCO₂and PO₂value for the actual patient temperature. Gas is less soluble (and therefore has a higher partial pressure) at higher temperatures in the bloodstream, therefore a blood sample from a hypothermic patient analysed at 37°C will overestimate the true PaCO₂or PaO₂. Depending on the concentration gradient between the blood sample and air bubbles, oxygen will diffuse into or out of the blood sample leading to either an increase or decrease in the measured PO₂. In extreme leukocytosis, oxygen consumption occurs and pseudohypoxaemia is seen.

1. Nickson C. Arterial blood gas in hypothermia. Life in the fast lane. http://lifeinthefastlane.com /education/ccc/arterial-blood-gas-in-hypothermia (accessed 3rd August 2014). 2. Bersten AD, Soni N. Oh’s Intensive Care Manual, 6th ed. Philadelphia, USA:

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Normal intracranial pressure is between 5 and 15mmHg. There are rhythmic variations in ICP, named Lundberg A, B and C pressure waves. Although B and C waves are associated with variations of respiratory movements and blood pressure, A (or plateau) waves are sustained elevations of intracranial pressure lasting for several minutes. They signify raised intracranial pressure. Sneezing, coughing and straining can increase ICP by 45mmHg.

Normal ICP waveforms are similar to the arterial waveform, with a first peak (P1, percussion wave) correlating with systole, a second peak (P2, dicrotic wave) which correlates with aortic valve closure, and a third peak (P3, tidal wave) correlating with antegrade arterial flow during diastole; as intracranial compliance falls, the morphology of the ICP waveform also changes, with the amplitude of the dicrotic wave, the second peak, initially equals and then exceeds the amplitude of the percussion wave.

The primary goal of ICP management is to maintain ICP below 20mmHg and cerebral perfusion pressure (CPP) above 60mmHg. While elimination of the cause of elevated ICP remains the definitive approach, there are interventions that should be used to decrease ICP urgently, while CPP management should be emphasised.

1. Sabdoughi A, Rybinnik I, Cohen R. Measurement and management of increased intracranial pressure. Crit Care Med J 2013; 6 (Suppl 1: M4): 56-65.

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Weaning from mechanical ventilation is the stepwise process of reducing respiratory support with the ultimate aim of extubation and satisfactory spontaneous breathing. Many critically ill patients will tolerate this process rapidly following improvement from their acute event. Some patients will need a more gradual approach.

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General features associated with successful weaning include improvement in the underlying condition, optimisation of general physiology and identification of potentially deleterious airway or breathing issues. Following this, numerical indices are a fairly reliable way of predicting the likelihood of success with a spontaneous breathing trial and have been consistently shown to outperform clinical judgement when used systematically.

Numerical indices in current use include the Rapid Shallow Breathing Index <105 (respiratory rate divided by tidal volume measured in litres), respiratory rate in isolation (<35/min), vital capacity >10ml/kg and PaO₂/FiO₂ >26kPa. However, there remain concerns regarding the sensitivity and specificity of chosen cut-offs and they must be used as part of a rational decision-making process, rather than as standalone targets. Isolated measurements of PO₂or CO₂have a limited role.

1. Lermitte J, Garfield MJ. Weaning from mechanical ventilation. Contin Educ Anaesth Crit Care Pain 2005; 5: 113-7.

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The Sengstaken-Blakemore tube is used in the temporary management of bleeding varices. It can be inserted orally or nasally and can be used in awake patients. The tube has oesophageal and gastric balloons and one port to aspirate gastric contents. The Minnesota tube has an additional port to aspirate oesophageal contents in an attempt to reduce the risk of aspiration pneumonia. The tube is inserted to the 55cm mark (indicating a position well below the gastro-oesophageal junction), the gastric balloon inflated with water or air, and the position checked with radiography. Once the position is confirmed the gastric balloon is completely inflated. The tube is then pulled back until resistance is felt. If bleeding continues, the oesophageal balloon can also be insufflated. Weighted traction using bags of saline is no longer recommended as it can lead to necrosis at the gastro-oesophageal junction and at the angle of the mouth. Traction on the tube is best applied using tape to the skin of the nose only. The use of a

Sengstaken-Blakemore tube is associated with serious complications such as oesophageal ulceration, oesophageal perforation and aspiration pneumonia in 15-20% of cases. Up to 50% of patients will rebleed once the balloon is deflated, so its primary function is to control bleeding prior to further definitive treatment.

1. Waldmann C, Soni N, Rhodes A.Oxford Desk Reference Critical Care. Oxford, UK: Oxford University Press, 2008.

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Among the common associated risk factors for development of acute kidney injury in the postoperative period are: pre-existing renal insufficiency; Type 1 diabetes mellitus; patient age over 65 years; major vascular surgery; cardiopulmonary bypass times over 3 hours; and recent exposure to nephrotoxic agents (such as radio-contrast dyes, bile pigments, aminoglycoside, antibiotics, and NSAIDs).

1. Sear JW. Kidney dysfunction in the postoperative period. Br J Anaesth 2005; 95(1): 20- 32.

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Continuous positive airway pressure has multiple physiological ramifications within the intensive care unit. While it may be a very familiar treatment, understanding of these effects will lead to best use in clinical practice.

Functional residual capacity (FRC) will impact on gas transfer due to an impact on alveolar surface area available for exchange. Positive end- expiratory pressure (PEEP) can reduce atelectasis and maintain recruitment of collapsed alveoli, thus increasing the FRC and subsequently increasing surface area for the transfer of oxygen to the bloodstream.

PEEP can also have important cardiovascular effects such as a reduction in preload, redistribution of extravascular lung water (secondary to

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increased hydrostatic pressure within the alveoli) and decreased left ventricular afterload. This latter feature has led some authors to suggest that PEEP can increase cardiac output, although the general consensus at present suggests that the impact of decreased preload and consequent decreased left ventricular filling cause little positive effect on cardiac output. In a small cohort of patients with a failing myocardium and hypervolaemia (congestive cardiac failure), PEEP may result in improved cardiac output due to the decrease in afterload providing greater overall benefit. There is trial evidence to support CPAP in this situation to reduce symptoms and work of breathing.

PEEP will invariably increase intracranial pressure by impairing venous drainage to the thorax, resulting in a degree of intracranial venous congestion and resultant pressure increase alongside volume expansion. 1. Luecke T, Pelosi P. Clinical review: positive end-expiratory pressure and cardiac output.

Crit Care 2005; 9(6): 607-21.

2. Gray A, Goodacre S, Newby DE, et al. Non-invasive ventilation in acute cardiogenic pulmonary oedema. New Engl J Med 2008; 359: 142-51.

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The neurological level of a spinal cord injury is defined as the lowest level of the spinal cord with normal sensation and motor function on both sides of the body. Due to secondary injury, cord ischaemia extends bi- directionally from the site of injury over the first 72 hours which may manifest as an ascending neurological level and lead to clinical deterioration. Spinal cord injuries above the level of T8 lead to impaired ventilation due to a loss of inspiratory intercostal and abdominal muscles. If the injury is between C3-5, there is partial phrenic nerve denervation and above C3, total diaphragmatic paralysis occurs. In a high spinal cord injury, lying flat improves respiratory function as the diaphragm has a greater excursion in inspiration as it is pushed into the chest by the abdominal contents. Gastroparesis may occur due to unopposed vagal activity. Feeding patients with high cord lesions enterally may lead to vomiting, abdominal distension and the risk of

aspiration; however, early enteral feeding has been shown to decrease mortality in polytrauma patients and enteral feed should be attempted within the first 24 hours after injury. Rates of deep vein thrombosis (DVT) are as stated. Intermittent calf compression devices or graduated compression stockings should be used as prophylaxis for DVT during the first 48-72 hours because of the risk of bleeding around the cord. After 72 hours, prophylactic low-molecular-weight heparin should be commenced, unless contraindicated due to other injuries. Acute denervation of the motor end plate leads to spread of acetylcholine receptors beyond the motor end plate and after 72 hours the use of suxamethonium may precipitate life-threatening hyperkalaemia. This effect resolves after approximately 6 months and suxamethonium can again be safely used.

1. Bonner S, Smith C. Initial management of acute spinal cord injury. Contin Educ Anaesth Crit Care Pain 2013; 13(6): 224-31.

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The acute management of Wolff-Parkinson-White (WPW) syndrome with tachycardia is divided into the following:

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Unstable: synchronised DC shock.

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Stable: anti-arrhythmic agents which cause prolongation of the accessory pathway such as sotalol, procainamide, flecainide and amiodarone.

There are important differences between the pathophysiology of regular narrow complex tachyarrhythmias in this condition compared with the tachyarrhythmia of atrial fibrillation (AF) with rapid ventricular response and this has implications for the drugs used to terminate acute episodes. In the case of atrioventricular reentrant tachycardias (AVRT) or AV nodal reentrant tachycardias (AVNRT), AV node-blocking drugs such as adenosine and verapamil can be used to break the cycle of reentrant electrical activity. However, the use of AV node-blocking drugs in atrial

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fibrillation with fast ventricular response is contraindicated, as in this situation atrial electrical activity will be conducted with greater frequency to the ventricles via the accessory pathway (since the AV node is blocked), risking increased ventricular rate and deterioration into a malignant rhythm.

β-blockers, digoxin, adenosine and verapamil all have a blocking action on the AV node and hence should be avoided. Amiodarone may also have a similar action and should be avoided in this situation also. Suitable agents include Class Ic drugs such as flecainide and propafenone, and Class III agents such as ibutilide.

The management and diagnosis of tachyarrhythmias in WPW syndrome is complex and expert advice should be sought if the patient is haemodynamically stable.

1. Di Biase L, Walsh EP. Treatment of symptomatic arrhythmias associated with the Wolff- Parkinson-White syndrome, 2014. UpToDate. http://www.uptodate.com/contents/ treatment-of-symptomatic-arrhythmias-associated-with-the-wolff-parkinson-white- syndrome (accessed January 2nd 2015).

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Major burns are associated with a significant incidence of death and disability, multiple surgical procedures, prolonged hospital stay and organ support. Critical care must be fastidious and aggressive. A recent Cochrane review assessing the use of antibiotic therapy to reduce the risk of burn wound infection found no benefit to the use of selective digestive tract decontamination (SDD). In fact, a statistically significant increase in the development of methicillin-resistant Staphylococcus aureus (MRSA) was noted.

Initial treatment consists of fluid replacement, wound care and organ support. Fluid prescription is still guided by the Parkland formula in the early stages of care, which suggests 3-4ml/kg/% TBSA burn over the first 24-hour period, with any prehospital fluid subtracted from the total, and

the first half given over the first 8 hours. When calculating total body surface area, erythematous regions are omitted unless there is additional blistering or underlying evidence of partial-thickness burns.

The Baux score approximates mortality risk using the formula: age of patient + percentage TBSA burned. A modified score has also been proposed adding an additional 17% for airway burns involvement. 1. Barajas-Nava LA, López-Alcalde J, Roqué i Figuls M, et al. Antibiotic prophylaxis for

preventing burn wound infection. Cochrane Database Syst Rev 2013; 6: CD008738. 2. Benson A, Dickson WA, Boyce DE. ABC of wound healing: burns. Br Med J 2006;

332: 649.

3. Roberts G, Lloyd M, Parker M, et al. The Baux score is dead. Long live the Baux score. A 27-year retrospective cohort study of mortality at a regional burns service. J Trauma Acute Care Surg 2012; 72(1): 251-6.

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The FAST (Face, Arm, Speech, Time to call 999) test is publicised in the UK to diagnose stroke. It has a positive predictive value of approximately 80%.

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