Educational Forum/Thread Game

[Scaramedic]

I thought this might be a fun way to further our education. The rules are simple, answer the question/define the term and leave a question/term for the next person. The question can be anything EMS; medical terms, EKG's, meds, diseases, anatomy, equipment, etc. Let's try to mix in both ALS & BLS, so everyone can be involved. This is an educational thread so don't feel bad looking it up and using Copy & Paste. Also please do not use obscure questions, I do not believe Craniofacial Dysostosis is relative to EMS. Finally lets keep it civil and have fun.

I'll get us started..

Stokes-Adams syndrome

Peace,

Marty

[Ace844]

What is a Stokes Adams attack?

If you have this condition, you usually lose consciousness for a short period of time - between 10 and 30 seconds. This is usually caused by a longer than normal pause between heartbeats. Most people regain consciousness rapidly when their pulse returns to normal. However, if you remain unconscious and your heart rate does not return to normal, this could lead to a cardiac arrest. This is where the heart stops beating, and you will need emergency life support. Stokes Adams attacks can occur in people with second degree or complete heart block, which are conditions where there is an abnormality in the heart’s electrical activity.

Stokes-Ad·ams syndrome (stksdmz)

n.

An occasional temporary stoppage or extreme slowing of the pulse as a result of heart block, causing dizziness, fainting, and sometimes convulsions. :wink: :shock:

ACE844

Try this one; what is HONK aka:Hyperosmolar Hyperglycemic Nonketotic Coma ?

[AZCEP]

H-O-N-K: Another in a long line of descriptions for Hyperglycemic (high blood sugar) Hyperosmolar (increased osmolar fluid loss) Non-Ketotic (no ketones produced) syndrome.

This is a sister syndrome to DKA, with a few differences.

1. No ketone production. These patients have just enough insulin available that the body does not utilize fatty acids for fuel sources.

2. Typically an older patient with pre-existing type II diabetes. Because of the usual regimen of insulin sensitizing agents, the body becomes more sensitive to the insulin that is available, and lesser amounts are released from the pancreatic beta cells. See #1

3. Higher blood sugars. DKA begins with BGL's of 250-300, and usually tops out in the 600-750 mg/dL range. HHNK, or HONK, will have blood glucose levels >800 mg/dL. Blood sugars in excess of 1000 mg/dL are not uncommon.

4. Ungodly amount of extremely dilute urine. DKA will run out of fluid, or the urine will become so concentrated with glucose and ketoacids the kidneys can't produce as much. HHNK will continually diurese the patient so the urine becomes diluted and it's specific gravity drops like a rock.

Management is focused on fluid replacement and normalizing the blood glucose level over an extended period. Too rapid a drop in blood sugar will cause just as many CNS dysfunctions as leaving it too high for too long. Usual rates of decrease are 100 mg/dL per hour until the blood sugar reaches 250 mg/dL.

QUESTION: What is the contraindication (relative or absolute) to the prehospital administration of oxygen? NOT ASSOCIATED WITH THE PATIENT BEING ON FIRE.

[Ace844]

H-O-N-K: Another in a long line of descriptions for Hyperglycemic (high blood sugar) Hyperosmolar (increased osmolar fluid loss) Non-Ketotic (no ketones produced) syndrome.

This is a sister syndrome to DKA, with a few differences.

1. No ketone production. These patients have just enough insulin available that the body does not utilize fatty acids for fuel sources.

2. Typically an older patient with pre-existing type II diabetes. Because of the usual regimen of insulin sensitizing agents, the body becomes more sensitive to the insulin that is available, and lesser amounts are released from the pancreatic beta cells. See #1

3. Higher blood sugars. DKA begins with BGL's of 250-300, and usually tops out in the 600-750 mg/dL range. HHNK, or HONK, will have blood glucose levels >800 mg/dL. Blood sugars in excess of 1000 mg/dL are not uncommon.

4. Ungodly amount of extremely dilute urine. DKA will run out of fluid, or the urine will become so concentrated with glucose and ketoacids the kidneys can't produce as much. HHNK will continually diurese the patient so the urine becomes diluted and it's specific gravity drops like a rock.

Management is focused on fluid replacement and normalizing the blood glucose level over an extended period. Too rapid a drop in blood sugar will cause just as many CNS dysfunctions as leaving it too high for too long. Usual rates of decrease are 100 mg/dL per hour until the blood sugar reaches 250 mg/dL.

QUESTION: What is the contraindication (relative or absolute) to the prehospital administration of oxygen? NOT ASSOCIATED WITH THE PATIENT BEING ON FIRE.

Paraquat-cumquat exposure... If this is correct, let me know and the next one is...

Kawasaki Disease ?

[AZCEP]

Very good Ace, but you didn't describe the why's and how's.

And it is Paraquat/diaquat exposure. Kumquats will only give you diarrhea.

[Ridryder 911]

Real Call this a.m. :7-6-06 0024 Responded to a 56 y.o. white female, with history of fever. F.D. upon scene and stated " family says her sugar was high (300 mg/dl) we repeated it & at was 200 for us. Patient somewhat sitting in upright position, (leaning over) on bed. Room dissarayed.

Presentation: 56 year old female grossly obese (>150 kg) very pale, extremely diaphoretic, distal extremities slightly dusky to taint cyanosis. Patient is awake however confused of surroundings, events.

Incident History : sister of patient (who herself appears to be in grave health) described that patient acutely became worse, FSBS performed. Patient was recently discharge from hospital 2 days ago with pneumonia.

History : Patient has outstanding history of COPD (asthma), CHF, Type II DM, HTN, etc...

Meds: Numerous, brief scan noted , Z-pack, home nebulizer fual med's, HCTZ, Lasix, NTG, Pepcid, Glucophage,Prednisone, home C-pap machince, etc...

Clinical findings: as noted intermittent <LOC, however responsive to stimulus and occasionally attempts to make jokes, skin cool, clammy. MMM pale, sticky, gummy. Pt. on 0[sub:f86d121fa8]2[/sub:f86d121fa8] @ 3 lpm N/C

Head , PEARLA @ 2.5 mm each, when responsive, EOM's intact, facial symmetry,

Chest: decreased t.v, hard to auscultate due to obesity and respiratory depth, however audible expiratory wheezes in upper lobes bi-lat., Hear tone rapid, clear with distinct S[sub:f86d121fa8]1[/sub:f86d121fa8] S[sub:f86d121fa8]2[/sub:f86d121fa8] without murmurs or clicks, APMI non-measurable at time.

Abdomen: as noted extremely obese, soft, palpable .. does c/o slight grimace with palpation of mid lower right hypochondriac region.

Extr.: anasarca, +3-4 edema , grade +1 pulses, clubbing noted @ 20 degrees

EKG: S.R. no noted ectopi, or ST elevations or axis deviation noted from XII lead.

S[sub:f86d121fa8]p[/sub:f86d121fa8])[sub:f86d121fa8]2[/sub:f86d121fa8]": initally 80% ETCo2: 35 mm/torr

V.S. BP 90 palpation Pulse 106-110, R/R 18-24

TX: FSBS checked 220 mg/dl, Oxygen increased to 15 lpm per NRBM, with preparation of CPAP, and possible RSI.

IV initiated with NSS bolus of 250 ml. Combi med's adm. per mask nebulizer, noted in creased tital volume as well as SpO2 incrasing to 94%, patient describing Sh.O.B decreasing. Ausculatation noted increased air movement with slight consolidation left lower lobe.

Repeated question of GI.. patietn admits having dark tarry stools lately ... ? predniosne =G.I. bleed ?

Advised ER of patient conditions of possible HHNC versus G/I bleed, COPD or all..

Outcome: patient was dx. with HHNC, placed on Insulin drip, after series of lab's, CT etc, small lower GI bleed detected as well as diffuse pulmonary infiltrates and tx with antibotics, RT tx'x, etc.... admitted to ICU with potential good prognosis

Hyperosmolar Hyperglycemic Nonketotic Coma

WOW ! or more commonly known as : :shock: HHNC, hyperosmolar coma, diabetic nonketotic coma, hyperosmolar nonketotic state, diabetic hyperosmolarity, diabetes, hyperglycemia, diabetic ketoacidosis, DKA, adult-onset diabetes, dehydration, sepsis, pneumonia, urinary tract infection, UTI, diuretics, beta-blockers, histamine 2 blockers, H2 blockers, stroke, intracranial hemorrhage, acute myocardial infarction, acute MI, acute heart attack, dialysis, gastrointestinal hemorrhage, hyponatremia....

Hyperosmolar hyperglycemic nonketotic coma (HHNC) is generally a metabolic derangement that occurs with patients with adult-onset diabetes (Type II non-Insulin dependent). The condition is characterized by hyperglycemia (usully > 200mg/dl although may not extrememly high), hyperosmolarity, and an absence of significant ketosis (such as ketones on breath/ Kussmaul's respirations).

According to e-med despite the name : ...."Coma is present in fewer than 10% of cases. Most patients present with severe dehydration and focal or global neurologic deficits. In many cases, the clinical features of HHNC and diabetic ketoacidosis (DKA) overlap and are observed simultaneously.....".

What happens pathophysio:: HHNC is most comon to develop in diabetic patients who have other illness that leads to a reduced fluid intake. Infection is the most common cause, but many other conditions can cause altered mentation and/or dehydration. Frequently, this other illness is not easily identifiable.

The hyperglycemia and hyperosmolarity lead to osmotic diuresis thus causing a big time osmotic shift of fluid to the intravascular space, resulting in further intracellular dehydration ( can you see the shock appearance?).

Patients with DKA, is not like patients with HHNC they do not develop ketoacidosis, but the reason for this is still not clear.

How often does this happen (frequency) In the US: The incidence is 17.5 cases per 100,000 people. This incidence is slightly higher than the incidence of DKA Although I believe it to be higher and often misdiagnosed.

Death Rate : The mortality rate is high (10-20%).

Sex: The prevalence is slightly higher in females than in males.

Age: High in the 70's but as earl y as children Residents of nursing homes are at the highest risk, but the syndrome has been reported in patients as young as 18 months.

Incident Preciding History: Most patients with HHNC have a known history of diabetes, which is usually Type II/ Non Insulin dependent

Often, a preceding illness results in several days of increasing dehydration.

Oral hydration usually is well because they ae unable to re-hydrate due to acute illness (eg, dementia, immobility, vomiting).

A divers neurologic changes may be present, including the following:

Decreased LOC such as drowsiness and lethargy

Confusion

Coma

Focal or generalized seizures

Visual changes or disturbances

Hemiparesis

Sensory deficits

Physical: The general appearance and hygiene may provide clues to the state of hydration (ion other words stinky!), presence of chronic illness, and reduced LOC.

Vital signs

As is seen in other dehydaration fast pulse (tachycardia) is an early indicator of dehydration; hypotension is a later sign suggestive of major dehydration.

Orthostatic vital signs (tilt test) are neither sensitive nor specific.

Fast respiratory rate (tachypnea) may result from respiratory compensation for metabolic acidosis.

High rectal temp: One should assess core temperature rectally. A high or low temperatures suggest sepsis.

Hypoxia can be a problem affecting mentation. Administer oxygen if the patient has any degree of desaturation or low sats'.

Perform a thorough assessment including skin examination searching for sources of infection, such as cellulitis or abscess.

Skin turgor is another clue to hydration status, with tenting (pulling of skin upright and staying there, good recoild is good turgor <3 seconds). Warm, moist skin suggests early sepsis where as cool, dry skin suggests late sepsis.

Exam of the head, eyes, ears, nose, and throat (HEENT) may reveal altered hydration status (eg, sunken eyes, dry mouth) mucus membranes sticky, gummy..

Cranial neuropathies should be evaluated in detail by the Paramedic such as :

.

Visual field losses and nystagmus sometimes are observed in HHNC.

The neck exam may reveal enlarged lymph nodes or meningismus. Palpation of the thyroid gland may reveal enlargement such as in thyrotoxicosis as a cause for tachycardia, fever, and dehydration.

The lung sounds or pulmonary and cardiac examinations may reveal signs of pneumonia or of cardiac diseases such as Congestive heart failure (CHF), acute respiratory distress syndrome (ARDS), or atypical pneumonia which can trigger HHNC.

Check for costovertebral angle (flank) tenderness as a sign of pyelonephritis (kidney area).

Look for Kernig and Brudzinski signs (nuchal rigidity), which may suggest meningitis.

A careful abdominal examination can help to rule out an intraperitoneal infection.

A later rectal examination can screen for prostatitis, perirectal abscess, and GI hemorrhage.

A later Pelvic examination is indicated in women with lower abdominal pain or purulent discharge.

Causes:

A current illness is common, but the underlying cause may be difficult to find. Pneumonia and urinary tract infections (UTIs) are the most common underlying causes of HHNC.

A wide variety of other major illnesses can cause HHNC causing no patient mobility and decrease water to drink SUch as .

Stroke, Acute myocardial infarction (MI), Gastrointestinal hemorrhage.

Stress response to any acute illness tends to increase the hormones that elevate glucose levels. Cortisol, catecholamines, glucagon, and many other hormones have effects that tend to counter those of insulin. Drugs that raise serum glucose, inhibit insulin, or cause dehydration may cause HHNC.

Such as

Diuretics (Lasix, Demadex, some bood pressure medications)

Beta-blockers

Histamine 2 (H2) blockers (sinus medications, antacids)

Patient being on dialysis, or having total parenteral nutrition (TPN)

Not compliant with oral hypoglycemics or insulin therapy.

Other Problems that need to considered or might mimick:

Delirium

Dementia

Overdose

Most of the time diagosis is usally based upon lab studies:

such as :

Serum electrolytes (sodium, potassium, chloride, bicarbonate) and calcium, magnesium, and phosphate

Hyponatremia or hypernatremia may be present.

In the setting of hyperglycemia, hyponatremia (low sodium) is more common due to the osmotic effect of glucose pulling water into the vascular spaces. The body potassium is likely low regardless of its serum value.An anion gap metabolic acidosis may be present because of dehydration (lactic acidosis) but usually is less profound than that observed in DKA.

Most patients who have hyperosmolar, hyperglycemic nonketotic have a component of DKA; therefore, ketoacidosis therefore you will have a anion gap acidosis.

Renal function (BUN (Blood Urea Nitrogen) basically waster prducts in the blood & creatinine levels) BUN and creatinine levels are likely to be elevated initially due to dehydration.

Creatine phosphokinase (CPK) with isoenzymes should be measured routinely because an AMI and rhabdomyolysis can trigger HHNC, and both can occur from the complications of HHNC.

Acute MI frequently is associated with HHNC.

Coagulation studies (Blood clotting) prothrombin time [PT] and activated partial thromboplastin time [aPTT]) are useful as part of a screen for disseminated intravascular coagulation (DIC).

Blood cultures should be obtained to search for bacteremia (bacteria) .

Arterial blood gases

ABG is the most accurate indicator of serum pH.

A

Urinalysis reveals elevated specific gravity (evidence of dehydration), glucosuria, ketonuria, and evidence of UTI.

Urine cultures are usedl because UTIs may be not seen by urinalysis alone, particularly in patients with diabetes.

Cerebrospinal fluid (CSF) fropm a lumbar spinal tap to check cell count, glucose, protein, and cultures.

Prehospital Care: Standard care for dehydration and decrease LOC. Airway management, IV access, Isotonic saline etc...

Comatose patients of course needs airway protection. Endotracheal intubation may be indicated. Measurement of ETCo2 may be an indicator of DKA versus Non-DKA.

Bolus of 500 mL of saline is appropriate for nearly all adult patients with dehydration. A 250 mL bolus may be more appropriate in patients with a history of CHF and/or renal insufficiency.

Basic medications given to most coma patients in the field may be thiamine 100 mg IV, dextrose (50 mL of D50), and naloxone (0.4-2 mg IV). This combination is of benefit to many comatose patients with few adverse effects.

Of course a fingerstick glucose measurement is obtained prior to dextrose administration.

Emergency Department Care: as per e-med.

Manage airway as needed, establish IV access, initiate vigorous fluid resuscitation, and obtain appropriate laboratory and radiographic studies.

Fluid deficits in HHNC are large; the fluid deficit of an adult may be 10 L or more.

Administer 1-2 L of isotonic saline in the first 2 hours. A higher initial volume may be necessary in patients with severe volume depletion. Slower initial rates may be appropriate in patients with significant cardiac or renal disease or in those who are not urinating.

After the initial bolus, some clinicians recommend changing to half-normal saline, while others continue with isotonic saline.

Either fluid likely will replenish intravascular volume and correct hyperosmolarity; a good standard is to switch to half-normal saline once blood pressure and urine output are adequate.

Once serum glucose drops to 250 mg/dL, the patient must receive dextrose in the IV fluid.

Initiate insulin therapy in the ED.

Although many patients with HHNC respond to fluids alone, IV insulin in dosages similar to those used in DKA can facilitate correction of hyperglycemia.

Insulin utilized without concomitant vigorous fluid replacement increases risk of shock.

Frequent reevaluation of clinical and laboratory parameters is necessary

During neurologic examination, evaluate overall mental status, cranial nerves, strength, sensation, reflexes, cerebellar function, stance, and gait. Focal findings may prompt further studies such as CT scan and/or lumbar puncture (LP).

Causes:

A preceding or intercurrent illness is common, but the underlying cause may be difficult to ascertain. Pneumonia and urinary tract infections (UTIs) are the most common underlying causes of HHNC.

A wide variety of other major illnesses may trigger HHNC by limiting patient mobility and free access to water.

Stroke

Intracranial hemorrhage

Acute myocardial infarction (MI)

Gastrointestinal hemorrhage

Stress response to any acute illness tends to increase hormones that favor elevated glucose levels. Cortisol, catecholamines, glucagon, and many other hormones have effects that tend to counter those of insulin.

Drugs that raise serum glucose, inhibit insulin, or cause dehydration may cause HHNC.

Diuretics

Beta-blockers

Histamine 2 (H2) blockers

Dialysis, total parenteral nutrition, and fluids that contain dextrose

Elder abuse and neglect also may contribute to underhydration.

Noncompliance with oral hypoglycemics or insulin therapy can result in HHNC.

[whit72]

Wait I think I know this one.

Kawasaki disease-

Is it the inflammation of the arteries, mainly in children? I also believe it affects the lymph nodes somehow but not sure exactly.

[Ace844]

Very good Ace, but you didn't describe the why's and how's.

And it is Paraquat/diaquat exposure. Kumquats will only give you diarrhea.

That's a great 'Pimp' question, and not many people ask it. I did a tox scenario here awhile ago related to this type of exposure and it seems to have disappeared, ... COULD ADMIN HELP??? here are some articles and links for those who are interested::

http://www.pubmedcentral.nih.gov/picrender...mp;blobtype=pdf

http://www.pubmedcentral.nih.gov/picrender...mp;blobtype=pdf

http://medind.nic.in/iav/t03/i2/iavt03i2p64.pdf

http://www.inchem.org/documents/pims/chemical/pim399.htm

http://www.pesticideinfo.org/Detail_Poison...?Rec_Id=PC33358

http://www.paraquat.com/portals/5/paraquat_booklet.pdf

ALSO,but it didn't come up on my search. I'll try again, until then...----->

Herbicide Poisoning

By Lewis Nelson, MD

One hour after intentionally ingesting two cups of an unidentified herbicide, a young woman presents to the emergency department complaining of vomiting, diarrhea, and throat pain. On physical examination, her initial vital signs are normal, as are her chest and abdomen, but her oropharynx is erythematous. Neither drooling nor stridor is present.

Because the patient has upper airway symptoms and signs of irritation, clearly the first priority must be to maintain airway patency. The decision to perform endotracheal intubation after a patient has ingested a caustic or irritating agent is often difficult. In addition to the obvious signs of airway compromise, the exact nature of the exposure may be the most important factor to consider. Patients who ingest highly caustic agents such as sodium hydroxide require aggressive airway management, since intubation may be extremely difficult once the airway becomes compromised. Identification of the specific exposure is therefore critical.

THE USUAL SUSPECTS

Although no longer available in the United States, paraquat carries the greatest morbidity and mortality among ingested herbicides. Paraquat is still a major cause of death and disability in some countries, such as Australia, and it was responsible for at least four deaths from acute poisoning in the United States in 1996. These consequences occur despite the fact that the chemical has been rendered technically "nontoxic" through the addition of emetic or malodorous agents, such as valeric acid.

Paraquat has an affinity for the lung, in which it is selectively absorbed and accumulates within type I and type II alveolar epithelial cells. Within these cells, paraquat generates oxygen free radicals that ultimately damage lipid membranes and cause cell death. The initial acute lung injury may progress to acute respiratory distress syndrome (ARDS); death occurs in more than 50% of patients after an intentional ingestion. Those patients who do survive enter a proliferative phase characterized by loss of alveolar integrity, proliferation of fibroblasts, and deposition of collagen, leading to pulmonary fibrosis.

Aggressive support is a must for patients who ingest paraquat. Ironically, oxygen supplementation may have a deleterious effect because it increases the number of toxic radicals. Oxygen should therefore be given only to prevent hypoxemia. Because paraquat is also corrosive, examination of the oropharynx and gastrointestinal system is critical. Gastrointestinal decontamination can be achieved with activated charcoal, bentonite, or fuller's earth, any of which will adsorb and inactivate the herbicide. Hemoperfusion may be effective in clearing systemic paraquat in patients who present soon after ingestion.

Diquat, a related agent, is readily available in the U.S. Although its herbicidal and toxic activity is similar to that of paraquat, it is not selectively concentrated in the lung and therefore is less toxic to the pulmonary system. However, diquat appears to be considerably nephrotoxic, an effect that may be related to its accumulation in the kidneys.

Chlorophenoxy derivatives such as 2,4-dichlorophenoxyacetic acid (2,4-D) are widely used by the general population as broadleaf weed herbicides. In fact, an estimated 60 million pounds are used in the U.S. annually by both homeowners and professional landscapers. Although 2,4-D is known as a component of the infamous herbicide Agent Orange, the chlorophenoxy herbicides are usually minimally toxic when ingested unintentionally in small quantities. Large ingestions, however, produce acute poisoning characterized by compromised mental status, seizures, cardiac arrhythmias, and rhabdomyolysis. Because these agents can uncouple oxidative phosphorylation and thereby cause cellular energy failure, death may occur.

Perhaps the most widely used garden herbicide in the U.S. today is glyphosate (brand name, Roundup). Although less toxic than the herbicides described above, glyphosate has been used in hundreds of deliberate self-poisonings worldwide. As an inhibitor of plant-specific amino acid biosynthesis, glyphosate should be minimally toxic to humans. In fact, its toxic effects may be related largely to the nonionic surfactant with which glyphosate is formulated.

The most pronounced effects include gastrointestinal irritation and erosion, although the oropharynx is also often affected. The involvement of the oropharynx may explain the relatively high incidence of pulmonary aspiration cited in many studies; however, acute lung injury may be induced through systemic effects as well. Profound hypovolemia may account for the hemodynamic abnormalities, although animal studies have also found that the surfactant may produce these effects directly. Supportive treatment should be given. Long-term adverse effects have not been noted among survivors of such glyphosate poisoning.

PARAQUAT OR GLYPHOSATE?

In countries such as China where both paraquat and glyphosate are used frequently, empiric therapy for both agents is often initiated. The epidemiology of the two agents, however, suggests that in the United States, glyphosate should be suspected whenever a patient presents with herbicide ingestion, since paraquat is virtually unavailable in this country. In some countries, the rapid urine screening test for paraquat is used routinely. The test involves the addition of dithionate to a urine sample, but the results may be negative for patients with sublethal ingestions. Nonetheless, it is important to make the differentiation between the two herbicides, either statistically or scientifically, since the therapies that may be considered for paraquat poisoning, such as hemoperfusion, are neither benign nor wise when administered to patients who are actually suffering from glyphosate poisoning.

In this case, the patient had ingested glyphosate. After undergoing endoscopy, which yielded normal results, she remained clinically stable and was discharged home after an overnight observation period.

Suggested Reading

Hung DZ, et al.: Laryngeal survey in glyphosate intoxication: a pathophysiological investigation. Hum Exp Toxicol 16:596, 1997.

Sawada Y, et al.: Probable toxicity of surface-active agent in commercial herbicide containing glyphosate. Lancet 1:299, 1988.

Tominack RL, et al.: Taiwan National Poison Center survey of glyphosate-surfactant herbicide ingestions. J Toxicol Clin Toxicol 29:91, 1991.

--------------------------------------------------------------------------------

Dr. Nelson is director of the medical toxicology fellowship and associate director of the New York City Poison Control Center. He is also an assistant professor in the department of surgery/emergency medicine at New York University School of Medicine.

Emerg Med 34(5):48-49, 2002

[Ridryder 911]

Kawasaki Disease: No not associated with motorcycles :roll:

One of the few disease they test on for RN boards. I am sure Dust has seen far more that I have.

Primary childhood disease, unsure etiology. Primary seen in Asian decent however not always, can be ethnic group. Can lead to vasculature problems (valves, arrhythmia's) such as cardiac if not treated. Usually signs & symptoms are a fever that will not disappear (>5 days), blood shot eyes, rash predominately on hands, enlarged lymph nodes, and chapped lips etc..

Treatment is usually gamma globin ..

I have seen 2 or 3 cases....very interesting presentations.

Okay here is an interesting one, we see a lot in ER.. 5'th disease.. ? Oh by the way what were the other 4 previously?

R/r 911

[Ace844]

"Ridryder 911,"

Great HONK case and very typical, great catch..!!!

ACE