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The three main groups of syncope, i.e. reflex, cardiovascular, and secondary to orthostatic hypertension (OH), are shown outside the rings in Figure 3 . Both reflex syncope and OH span the two main pathophysiological mechanisms.

Figure 3
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Pathophysiological basis of the classification of syncope.

ANS = autonomic nervous system; auton. = autonomic; BP = blood pressure; OH = orthostatic hypotension; periph. = peripheral; resist. = resistance.

Figure 3
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Pathophysiological basis of the classification of syncope.

ANS = autonomic nervous system; auton. = autonomic; BP = blood pressure; OH = orthostatic hypotension; periph. = peripheral; resist. = resistance.

Only those forms of epilepsy in which normal motor control is lost, so patients may fall, are included in Figure 2 . These are tonic, clonic, tonic−clonic, and atonic generalized seizures, and can be classified as primary or secondary. The forms of epilepsy in which people remain actively upright, i.e. sitting or standing (e.g. complex partial seizures or absence epilepsy) are not regarded as TLOC, but sometimes they are incorrectly diagnosed as syncope.

Psychogenic TLOC consists of two forms: one resembles epileptic seizures (psychogenic non-epileptic seizures [PNES]) and one, without gross movements, resembles syncope (psychogenic pseudosyncope [PPS]).

The rare causes of TLOC only seldomly cause confusion with the main TLOC forms, probably because in most cases they differ enough clinically to be clearly not syncope. Both vertebrobasilar transient ischaemic attacks (TIAs) and subclavian steal syndrome are associated with focal neurological signs. A subarachnoid haemorrhage may present with a short LOC, but the associated abrupt extreme headache suggests the cause. In cyanotic breath-holding spells, expiratory apnoea with hypoxia is the primary mechanism. 10 So-called ‘pallid breath-holding spells’ in children do not constitute a primary respiratory problem, but are cardioinhibitory reflex syncope. 11

Table 4 lists the main features that distinguish syncope from disorders that may be mistaken for syncope.

Table 4

Conditions that may be incorrectly diagnosed as syncope

LOC = loss of consciousness; PPS = psychogenic pseudosyncope; TIA = transient ischaemic attack; TLOC = transient loss of consciousness.

Table 4

Conditions that may be incorrectly diagnosed as syncope

LOC = loss of consciousness; PPS = psychogenic pseudosyncope; TIA = transient ischaemic attack; TLOC = transient loss of consciousness.

The clinical features characterizing TLOC are usually derived from history taking from patients and eyewitnesses. When a patient first presents with possible TLOC, history taking should first establish whether there was indeed a TLOC. Often, this allows a distinction between the major TLOC groups. The flow diagram for the evaluation of TLOC is shown in Figure 4 . The initial evaluation should answer key questions:

In their survey, Turner and company found one phage that infected P. aeruginosa by grabbing on to part of this pump, a part called the outer membrane porin M. The phage was collected from Dodge Pond, about 65km east of Yale. The researchers dubbed it OMKO1 or outer-membrane-porin M knockout dependent phage #1.

If the deadly bacteria have the pump, the phage can grab hold and kill them. If the bacteria lack the pump or have a mutant, broken version, that means that phage can’t get in and kill—but standard antibiotics can.

In early lab tests, Squad Slogan Black High Waisted High Leg Bikini Bottom Pretty Little Thing Official For Sale Outlet Fake AqOBe
, Turner and his lab showed that as P. aeruginosa evolved resistance to OMKO1, it became more susceptible to antibiotic treatments. To verify that this phage could one day be clinically useful, they tested it out on several P. aeruginosa strains that Yale colleagues had isolated from patients—including one who had a chronic infection on an aortic arch graft.

As Turner and his lab carried out their work, the doctor’s health continued to slip. Doctors and researchers made the bold decision to try out the phage. Turner’s lab collected bacteria-laden discharge from a fistula that formed in the doctor’s chest and mixed it with phage. The pond virus killed off most of the bacteria and re-sensitized the survivors to antibiotics. With such promising lab results, the team got an emergency investigational new drug approval from the Food and Drug Administration to treat the sick doctor with their pond phage.

With the doctor’s aorta seemingly disintegrating, Narayan and Turner’s teams injected a high dose of purified OMKO1 in combination with the antibiotic ceftazidime directly into the fistula in his chest.

The next day, the doctor had stable vital signs and had no complaints. He was subsequently released from the hospital. Things were looking up until four weeks later, when his chest wound started bleeding. Doctors had no choice but to perform emergency surgery. With his chest open, the surgeons found that a bone fragment from his sternum had broken off and pierced his aorta. But what they didn’t find was any evidence of a P. aeruginosa infection. The surgeons repaired damage and replaced the aortic graft. Shortly after, they took him off antibiotics and he has been off them ever since.

The researchers concluded that the phage was critical for ridding the doctor of his deadly infection. “Eventual controlled trials examining phage application as adjunctives may reveal improved clinical outcomes in cases of recalcitrant infection,” they wrote.

For now, they conclude, “the current case study indicates the fortuitous possibility for a single phage to apparently resolve the bacterial infection, where pre-treatment understanding of the evolutionary mechanism… underlying bacterial resistance informed the choice of phage used in experimental therapy.”

Evolution, Medicine, and Public Health , 2018. DOI: 10.1093/emph/eoy005 ( About DOIs ).

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