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Wikimedia Commons. Liverpool 1st title — Manchester United 13 titles. Season Champion 1. Season Champion Manchester United.
Arsenal a, b. Aston Villa a, c. Burnley c. Chelsea a, b. Crystal Palace a. Everton a, b, c. Liverpool a, b.
Manchester City a. Manchester United a, b. Raphael Honigstein forecasts another frustrating year for Arsenal and Mesut Ozil.
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FC Watford. Allgemein Jetzt downloaden! Zverev Texas Hold Em Karten Nowitzki im Karriere-Quiz min. Markedly elevated Factor VIII levels may tend to pull the aPTT downwards.
Thromboelastography TEG Panigada et al. Antithrombin levels may be slightly diminished. Factor VIII and von Willebrand factor are considerably increased.
CT pulmonary angiography May be useful in select patients. Logistically, large-volume CT scanning of patients with COVID is often impossible e.
In ICU patients, this is a very common problem. For patients on a heparin infusion, heparin resistance will be clinically obvious due to inability to achieve a therapeutic PTT level or an anti-Xa level.
For patients who are being treated with low molecular-weight heparin LMWH , heparin resistance may go unnoticed.
This may cause LMWH therapy to be ineffective. Further discussion of heparin resistance in general here , and more evidence on heparin resistance in COVID is here.
DVT prophylaxis DVT prophylaxis should generally be maintained — unless platelets are below Consequently, these authors suggested doubling the typical dose of prophylactic heparin e.
Spiezia L et al. Dutt et al. This provides biological evidence of heparin resistance, explaining the clinical failure of standard DVT prophylaxis observed across many trials.
Moll et al. How should DVT prophylaxis in the ICU be provided? This is currently unclear. This dosing scheme is already supported by a considerable body of evidence in other types of critically ill patients discussed further here.
Based on heparin resistance, standard doses of low molecular weight may be inadequate among critically ill patients e.
It could be preferable to use a heparin infusion if this is feasible, as it will ensure that therapeutic heparin efficacy is achieved.
Lin et al. Most critically ill patients with COVID are hypercoagulable and heparin-resistant. Therefore, a standard therapeutic dose of low molecular-weight heparin e.
In addition to prevention of thrombosis, heparin could reduce cytokine levels, thereby improving systemic inflammation Shi et al.
Further discussion of multiple possible benefits of heparin in COVID in this article by Thachil. The optimal dose of anticoagulation remains unknown at this point in time, with RCTs ongoing.
Currently it may be best to individualize the dose, based on weighing the risks of hemorrhage versus thrombosis. This could be considered for a patient who was peri-arrest with a high suspicion for pulmonary embolism.
RCTs may be warranted to evaluate this further. Diagnosis is clinical based on characteristic appearance of the extremities as well as laboratory derangements e.
Treatment of purpura fulminans is challenging. For a discussion of this, see the chapter on purpura fulminans.
SARS has been shown to induce a transient state of insulin resistance. Currently there isn't any evidence available regarding COVID Possible predictions regarding COVID??
Currently these are guesses. Prolonged use of some medications may cause dependence and even withdrawal e. This may necessitate a transition to oral agents which seem to be in better supply.
One example of an analgosedative ladder for COVID is shown below; For ongoing pain, analgesics are added on sequentially.
For ongoing anxiety, sedatives are added on sequentially. A surprising number of patients can be rendered awake and comfortable on the ventilator with this combination especially when using a comfortable ventilator mode, such as APRV.
In cirrhosis or severe alcoholism, the dose may be cut in half mg q6hr. Acetaminophen provides mild analgesia as well as antipyresis both effects with a goal of improving patient comfort.
This isn't a real reason to use ketamine, but perhaps a fringe benefit. The usual dose is 0. At the higher end of this range, mild psychotomimetic effects may be seen.
These effects are often beneficial e. Empirical dose-titration can generally find a sweet spot where there is analgesia, but no problematic psychotomimetic side-effects.
When in doubt, it's safer to stay closer to the 0. Thus, it's probably preferable to use large PRN boluses, compared to a continuous infusion.
Opioid infusions are prone to numerous problems: They tend to run longer and at higher doses than necessary, thereby increasing toxicity. Fentanyl tends to accumulate in fat tissue over time, which can be extremely problematic.
Fentanyl infusions expose patients to massive cumulative doses of opioid e. If opioid infusions are used, a daily interruption or dose-reduction should be performed to verify that the dose of opioid being used is indeed necessary.
For patients on an opioid infusion, always ensure that a substantial amount of opioid e. The usual dose is 5 mg QHS.
Olanzapine The major advantage of olanzapine is that it doesn't prolong QT or cause Torsades de Pointes. The most logical dosing schedule might be mg QHS.
The drawback of olanzapine is that it has a relatively low maximum dose 20 mg , which may limit its potency. At these doses, it may be a bit more powerful than olanzapine.
The drawback of quetiapine is that it does increase the QT interval. Quetiapine has a shorter half-life than olanzapine, so it should be dosed twice daily for use as a maintenance sedative.
A higher dose may be given at night to promote sleep e. Propofol infusion is generally preferable here. COVID patients appear prone to developing hypertriglyceridemia due to propofol possibly because of underlying hemophagocytosis.
This is problematic, because severe hypertriglyceridemia may necessitate completely stopping propofol. Using low doses of propofol e.
Haloperidol may increase the QT interval, so caution is required. However, as we encounter shortages of other sedatives, low-dose phenobarbital as an adjunctive, general-purpose sedative may become increasingly useful Gagnon et al.
Due to balanced effects on the glutamate and GABA systems, phenobarbital may be less deleriogenic than benzodiazepines.
Sometimes PRN benzodiazepines are necessary. In this situation, the dose of benzodiazepine should be minimized. Simultaneous efforts should be made to augment other sedatives and analgesics, with a goal of minimizing benzodiazepine exposure.
It will be difficult sorting out common complications of critical illness versus unique features of COVID Aaroe et al. Toscano et al.
Weakness is the predominant clinical finding most often ascending paralysis. Dysautonomia doesn't seem to be a prominent issue.
The diagnosis may be supported by neuroimaging excluding other lesions and bedside electrophysiologic studies. Intravenous immune globulin IVIG is generally the front-line therapy for Guillain-Barre Syndrome with equal efficacy compared to plasmapheresis and superior tolerability.
More on GBS in the IBCC chapter on this here. Acute Disseminated Encephalomyelitis ADEM This has been reported only in a single patient with COVID, so its incidence remains unclear Zhang et al.
Acute Disseminated Encephalomyelitis is often seen after viral illnesses. It causes multifocal demyelinating lesions scattered throughout the white matter within the brain, spinal cord, and optic nerves.
A variety of symptoms may occur, depending on the location of the lesions e. The diagnosis is based largely on neuroimaging with multiple lesions present, resembling those of multiple sclerosis.
This may be treated with steroid. Acute necrotizing encephalopathy This is a rare disorder caused by various viral infections. It has been reported in only a single patient with COVID, so its incidence in this situation remains unclear Poyiadji et al.
The pathogenesis seems to involve systemic inflammation, which damages the blood-brain barrier Wu et al. Clinical features may include confusion, seizure, or focal neurologic deficits.
Radiographically this causes multi-focal, symmetric lesions on CT scan and MRI involving the thalami, brainstem, cerebral white matter, and cerebellum with involvement of the bilateral thalami being the most consistent finding.
At various stages, there may be edema, petechial hemorrhages, or eventually necrosis. There is no established therapy.
Steroids have been utilized with mixed results. However, it seems that COVID causes an unusually large number of ischemic strokes including in patients with otherwise mild disease manifestations.
This is likely a manifestation of hypercoagulability due to COVID Oxley et al. Aside from stroke, these patients had either none or mild symptoms from COVID Viral encephalitis COVID can invade the brain and directly cause a viral encephalitis.
Fortunately this seems to be rare. To date, only one case of encephalitis is reported Moriguchi et al. ECMO back to contents Patients with COVID can be relatively young and suffering from single-organ failure due to a reversible etiology, so many would be excellent candidates for ECMO.
VV ECMO could be used for respiratory failure although it's unclear how common true refractory hypoxemia is. VA ECMO could be useful in patients with fulminant cardiomyopathy and cardiogenic shock Exact indications and timing are unclear.
In an epidemic, ECMO capabilities would probably rapidly become saturated. Very thorny ethical issues could arise e.
However, D-dimer values vary between labs, clouding generalization of this data. However, ferritin may lab behind current clinical changes and is often harder to obtain rapidly, making it less useful for acute risk stratification.
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