cefepime, ceftazidime, imipenem, meropenem or piperacillin–tazobactam; plus
ciprofloxacin, levofloxacin, amikacin, gentamicin, or tobramycin; plus
linezolid or vancomycinIn one observational study, empirical antibiotic treatment that was not according to international treatment guidelines was an independent predictor of worse outcome among HCAP patients.Guidelines from Canada suggest that HCAP can be treated like community-acquired pneumonia with antibiotics targeting Streptococcus pneumoniae, based on studies using blood cultures in different settings which have not found high rates of MRSA or Pseudomonas.Besides prompt antibiotic treatment, supportive measure for organ failure (such as cardiac decompensation) are also important. Another consideration goes to hospital referral; although more severe pneumonia requires admission to an acute care facility, this also predisposes to hazards of hospitalization such as delirium, urinary incontinence, depression, falls, restraint use, functional decline, adverse drug effects and hospital infections. Therefore, mild pneumonia might be better dealt with inside the long-term care facility. In patients with a limited life expectancy (for example, those with advanced dementia), end-of-life pneumonia also requires recognition and appropriate, palliative care. Prognosis
Healthcare-associated pneumonia seems to have fatality rates similar to hospital-acquired pneumonia, worse than community-acquired pneumonia but less severe than pneumonia in ventilated patients. Besides clinical markers like tachypnea (fast breathing) or a high white cell count (leukocytosis), the prognosis seems to be influenced by the underlying associated diseases (comorbidities) and functional capacities (for example, the ADL score). Many patients have a decreased health condition after the episode.
Paroxysms of laughter have no relation to the EEG, ruling out this feature as a gelastic phenomenon.EEG anomalies may be used as a quantitative biomarkers to "chart progression of AS and as clinical outcome measures". Slow delta activity (~3 Hz) is greatly increased in AS relative to typically developing children, yet more pronounced in children with partial 15q deletions as opposed to those with etiologies principally affecting UBE3A. Theta activity (~5 Hz) is much greater in children with partial 15q deletions. Thus, delta activity appears to be chiefly reflective of UBE3A dysfunction with some modulation from other 15q genes, whereas theta activity may be an electrophysiological readout of genes beyond UBE3A such as GABRA5, GABRB3, and GABRG3. Future clinical trials in AS might exploit the foregoing by using EEG as a readout of drug target engagement.It appears that the neurons of people with Angelman syndrome are formed correctly, but they cannot function properly. Diagnosis
The diagnosis of Angelman syndrome is based on:
A history of delayed motor milestones and then later a delay in general development, especially of speech
Unusual movements including fine tremors, jerky limb movements, hand flapping and a wide-based, stiff-legged gait. Characteristic facial appearance (but not in all cases). A history of epilepsy and an abnormal EEG tracing.