ICU Flashcards
Define head injury
severity and %
trauma to the head other than superficial injuries to the face
Mild head injury makes up around 90% (GCS 13-15),
moderate 5% (GCS 9-12)
severe head injury 5% (GCS ≤8).
Head injury how is autoregulation affected
head injury the normal autoregulation of cerebral blood flow (CBF) is lost
and
CBF becomes proportional to
cerebral perfusion pressure (CPP),
which in turn is directly determined by
both the mean arterial pressure (MAP) and the intracranial pressure (ICP):
CPP = MAP − ICP
Target MAP in head injury
greater than 80-90 mmHg
until ICP monitoring is established,
and assumes that the ICP is 20 mmHg and
therefore ensures a CPP of at least 60-70 mmHg.
Gold standard for ICP
An external ventricular drain (EVD) is perhaps the gold standard method of measuring ICP via an intraventricular catheter.
Name some indications for CTB
The following indications for performing a head scan in head-injured patients are provided by the National Institute for Clinical Excellence (NICE) in the UK:
GCS less than 13 at any point since injury
GCS equal to 13 or 14 at two hours after injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture
Post-traumatic seizure
Focal neurological deficit
More than one episode of vomiting, and
Amnesia of events, for greater than 30 minutes before impact.
TPN
What is required
How is the nitrogen component given
The principles of total parenteral nutrition (TPN)
involve calculating nitrogen balance, energy, fluid and electrolyte requirements.
TPN
what electrolytes should be given with tpn and how much per gram N
The nitrogen component should be given as mixtures of both essential and non-essential amino acids. 5-6 mmol of potassium and 1-2 mmol of magnesium (not calcium) are required per gram of nitrogen.
TPN
how is carb given
How is fat given
Carbohydrate is usually given as glucose (10 to 50%), but other energy sources e.g. ethanol, xylitol and sorbitol have been used.
Fat is usually administered as 10 or 20% soya bean oil emulsion.
Trace elements and minerals must also be added.
Metabolic complications of TPN include: x4
hypophosphataemia
hypernatraemia
hyperglycaemia, and
lipaemia.
NIV and aerosol
is ppe required?
how can aerosols be reduced at commencement
where should patient be nursed
Whilst there is no evidence that NIV prevents invasive ventilation in H1N1 patients, it is commonly used as bridging therapy. It is important to remember that these are open circuits and still require personal protection for staff.
Ensuring that a well fitting mask is in place before airflow starts can reduce the amount of aerosol production. Similarly, avoiding water humidification and use of a closed hood is also advised.
Ideally patients should be nursed in a negative pressure room.
HypoMagnesimia ECG changes
ECG changes of hypomagnesaemia are almost the same as those of hypokalaemia:
Flattening of T waves ST segment depression Prominent U waves Prolonged PR interval, and Prolonged QT interval
Hypo Mg risks
Atrial and ventricular arrhythmia
Affect of chronic hypomagnesaemia,
how may hypoMg occur
there is impaired synthesis and
release of parathyroid hormone (PTH),
and target organ response to PTH is impaired.
This produces secondary hypocalcaemia.
Hypomagnesaemia may result (like hypokalaemia) from the use of potassium ‘wasting’ diuretics (loop diuretics and thiazides, for example, furosemide).
Diagnostic “ Berlin” criteria of ARDS include:
1) acute onset, meaning onset over 1 week or less
2)
bilateral opacities consistent with pulmonary edema must be present and may be detected on CT or chest radiograph
3)
PF ratio <300mmHg with a minimum of 5 cmH20 PEEP (or CPAP)
4)
“must not be fully explained by cardiac failure or fluid overload,” in the physician’s best estimation using available information - an “objective assessment” (e.g. echocardiogram) should be performed in most cases if there is no clear cause such as trauma or sepsis.
The ARDSnet criteria recommend (vent parameters)
The ARDSnet criteria recommend
using tidal volumes of 6 ml/kg ideal body weight,
keeping plateau pressures <30 cmH2O,
using PEEP to optimise oxygenation
keeping the PaO2 above 8 kPa.
Common criteria
Caused by sepsis, trauma, direct lung injury and pancreatitis.
ARDS ddx and how it differs
x 3
Aspiration pneumonitis often preferentially affects dependent lung segments. Global, disseminated CXR changes are less likely than with ARDS.
Although basal atelectasis may account for some hypoxaemia it would not account for global CXR changes in middle and upper lung fields.
Cardiogenic pulmonary oedema is a key differential and can be diagnostically difficult to differentiate from ARDS as pulmonary artery catheters are rarely inserted. However, in this patient there is no history of acute cardiac disease and there is a good history of a common trigger for ARDS. Therefore ARDS is more likely than cardiogenic pulmonary oedema in this case
The initiation of emergency renal replacement therapy is usually required for:
Acute life threatening hyperkalaemia which is resistant to treatment. In this example the potassium is within normal limits.
Development of metabolic acidosis which is non-responsive to fluid. In this instance the pH is within normal limits.
Development of fluid overload, which may manifest itself as pulmonary oedema.
Development of uraemia which may manifest itself as pericarditis (not pancreatitis), neuropathy and confusional state.
Serotonin syndrome is characterised
Serotonin syndrome is characterised
by the triad of
1] altered mental status
(agitation, anxiety, restlessness and anxiety),
2] neuromuscular abnormalities
(tremors, clonus, muscle rigidity, akithisia and hyperreflexia)
3] Autonomic hyperactivity
(tachycardia, hypertension, sweating, hyperpyrexia, vomiting and diarrhoea).
It is most likely to develop within 24-hours of initiation of treatment.
Serotonin syndrome is characterised
Serotonin syndrome is characterised
by the triad of
1] altered mental status
(agitation, anxiety, restlessness and anxiety),
2] neuromuscular abnormalities
(tremors, clonus, muscle rigidity, akithisia and hyperreflexia)
3] Autonomic hyperactivity
(tachycardia, hypertension, sweating, hyperpyrexia, vomiting and diarrhoea).
It is most likely to develop within 24-hours of initiation of treatment.
Serotonin syndrome
Serotonin syndrome is a potentially life threatening adverse drug reaction that is a predictable consequence of excess serotonergic receptor agonism.
It produces a wide spectrum of clinical findings and commonly occurs within five weeks of commencing the drug
Patients with anticholinergic poisoning have normal reflexes, mydriasis, agitated delirium, urinary retention and hot, dry, erythematous skin
Neuroleptic malignant syndrome
Neuroleptic malignant syndrome is an idiopathic reaction to dopamine antagonists and is defined by slow onset developing over a period of days to weeks. It is characterised by neuromuscular hypoactivity (rigidity and hyporeflexia).
The RIFLE criteria uses changes in serum creatinine,
The RIFLE criteria uses changes in serum creatinine, GFR or urine output to categorise acute kidney injury into risk, injury and failure followed by loss and end stage categories for outcomes.
Risk correlates to:
creatinine increase of ×1.5
GFR decrease >25%, or
urine output <0.5 ml/kg/hr for six hours.
Injury correlates to:
creatinine increase of ×2
GFR fall of >50%, or
urine output <0.5 ml/kg/hr for 12 hours.
Failure correlates to:
creatinine increase of ×3
GFR fall of >75%
urine output <0.3 ml/kg/hr for 24 hours, or
12 hours of anuria.
Loss is complete loss of renal function for >4 weeks.
End stage is complete loss of renal function for >3 months.
OD TCA
In overdose tricyclic antidepressants cause central nervous system and cardiovascular effects and should be suspected in the presence of a prolonged QRS. The combination of seizures, altered level of consciousness and cardiac toxicity is classical. These features are caused mainly by a combination of anticholinergic effects and the inhibition of re-uptake of norepinephrine and serotonin.
Alcohol intoxication can cause a metabolic acidosis and seizures but ECG changes are unlikely.
Seizures and altered level of consciousness may be a feature of opioid poisoning but pupils are more likely to be constricted and cardiac toxicity is not usually seen.
Diabetic ketoacidosis can cause a metabolic acidosis with elevated anion gap. It would be unusual for pupils and ECG to be affected.
Lithium toxicity is incorrect as a decreased anion gap is usually seen.
The UK Resuscitation Council’s guidelines on the management of cardiac arrest in hypothermic patients differ slightly from the standard algorithm.
The UK Resuscitation Council’s guidelines on the management of cardiac arrest in hypothermic patients differ slightly from the standard algorithm.
In a patient with a core temperature below 30°C:
A total of 3 × DC shocks should be administered if on the shockable side of the algorithm (VF/VT)
Further shocks are not recommended until the patient is rewarmed to more that 30°C as the rhythm is refractory and so is unlikely to change
No drugs should be given as they will be ineffective.
In a patient with a core temperature between 30°C and 35°C:
DC shocks can be continued as normal
The time taken between drug doses should be doubled as they are metabolised much more slowly.
The patient should be actively rewarmed and protected against hyperthermia.
There is not enough information to know whether the resuscitation should be stopped so option e is false.
