User:Feldpama/sandbox


 * *Reflection of Wiki (below), Edited article (under this reflection)*

Reflection on Wiki

 * 1) Critiquing articles: What did you learn about Wikipedia during the article evaluation? How did you approach critiquing the article you selected for this assignment? How did you decide what to add to your chosen article?
 * 2) * Through the article evaluation, I learned about some of the rules regarding editing or creating Wikipedia pages. For example, the types of appropriate medical sources Wikipedia allows and how they like their articles formatted. I also learned that many articles lacked correct or appropriate sources; this lead me to focus on correct sourcing when I added information to my article. I wanted my sources to be credible so that I would convey correct and accurate information to readers.
 * 3) * To begin critiquing my article, I looked back on the rules/guidelines Wikipedia created, and I also used my knowledge and accurate sources to determine what information was lacking from the article. I decided that I wanted to reorganize the article a little to make it more "viewer friendly", and I also wanted to add additional signs/symptoms and risk factors for the disease I chose to write about (Hyperosmolar hyperglycemic state (HHS)).
 * 4) Summarizing your contributions: include a summary of your edits and why you felt they were a valuable addition to the article. How does your article compare to earlier versions?
 * 5) * For the article "Hyperosmolar hyperglycemic state", I added additional signs and symptoms such as polyphagia, dehydration, weight loss, nausea, vomiting and weakness. I also added additional risk factors for developing HHS because I felt that knowing the symptoms and risk factors of a disease are both important for the readers and potential victims to help educate them properly on what the disease entails. Also, I added information on how HHS compares and differs from Diabetic Ketoacidosis (DKA). I felt this was important because it allows viewers to better understand how these two similar diseases can be differentiated. Lastly, I added some information to the "Electrolyte replacement" section to clarify that potassium levels are often high or normal in HHS but they will lower once insulin therapy begins (the article had previously mentioned that potassium levels will only be low).
 * 6) Peer Review: If your class did peer review, include information about the peer review process. What did you contribute in your review of your peers article? What did your peers recommend you change on your article?
 * 7) * I think my peers would say I contributed valuable and important information to my article. I feel like maybe they would mention finding more sources to support the information I added because I had taken all of my information from only one source.
 * 8) Feedback: Did you receive feedback from other Wikipedia editors, and if so, how did you respond to and handle that feedback?
 * 9) * I received a little feedback on my article relating to the format of the piece. The editor mentioned to only capitalize the first word of every header, and to rarely using bolding/underlining in the articles. I responded well to the editors comments and fixed what he told me to.
 * 10) Wikipedia generally: What did you learn from contributing to Wikipedia? How does a Wikipedia assignment compare to other assignments you've done in the past? How can Wikipedia be used to improve public understanding of our field/your topic? Why is this important?
 * 11) * From contributing to Wikipedia, I learned that there was a bigger process involved in the editing and creating articles than I thought. I feel like this assignment differs from previous assignments I have done in the past because it involves editing/creating work for such a big audience to see! I am used to only showing my work to professors or peers, so I felt that there was added pressure to contribute correct and valuable information to my article. I think Wikipedia can improve understanding of my topic which is important because this disease that I wrote about (HHS) is a major complication of diabetes, and therefore, individuals should be educated on how this disease occurs, and what to expect if it does.

= Hyperosmolar hyperglycemic state = Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis.[4] Symptoms include signs of dehydration, weakness, legs cramps, trouble seeing, and an altered level of consciousness.[2] Onset is typically over days to weeks.[3] Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis.[2]The main risk factor is a history of diabetes mellitus type 2.[4]Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1.[3][4] Triggers include infections, stroke, trauma, certain medications, and heart attacks.[4] Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), osmolarity greater than 320 mOsm/kg, and a pH above 7.3.[2][3]Initial treatment generally consists of intravenous fluids to manage dehydration, intravenous insulin in those with significant ketones, low molecular weight heparin to decrease the risk of blood clotting, and antibiotics among those in whom there is concerns of infection.[3] The goal is a slow decline in blood sugar levels.[3] Potassium replacement is often required as the metabolic problems are corrected.[3] Efforts to prevent diabetic foot ulcers are also important.[3] It typically takes a few days for the person to return to baseline.[3]While the exact frequency of the condition is unknown, it is relatively common.[2][4] Older people are most commonly affected.[4] The risk of death among those affected is about 15%.[4] It was first described in the 1880s.[4]

Signs and symptoms[edit source]

Symptoms include:

·       Altered level of consciousness

·      Symptoms of high blood sugar, including increased thirst (polydipsia) and increased volume of urination (polyuria), and polyphagia (extreme hunger)

·      Neurologic signs including sensory or motor impairments,

·       Blurred vision

·       Headaches

·       Focal seizures, myoclonic jerking, reversible paralysis

·       Motor abnormalities including flaccidity, depressed reflexes, tremors or fasciculations

·       Hyperviscosity and increased risk of blood clot formation

·       Dehydration, weight loss

·       Nausea/vomiting/abdominal pain, weakness, and orthostatic hypotension.

Cause[edit source]

The main risk factor is a history of diabetes mellitus type 2.[4] Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1.[3][4] Triggers include infections, stroke, trauma, certain medications, and heart attacks.[4]

Additional Risk Factors:

-Lack of sufficient insulin (but enough to prevent ketosis)

-Poor kidney function

-Poor fluid intake (dehydration)

-Older age (50-70 years)

-Certain medical conditions (cerebral vascular injury, myocardial infarction, sepsis)

-Some medications (glucocorticoids, beta-blockers, thiazide diuretics, calcium channel blockers, phenytoin)

Pathophysiology[edit source]

HHS is usually precipitated by an infection,[5] myocardial infarction, stroke or another acute illness. A relative insulin deficiency, leads to a serum glucose that is usually higher than 33 mmol/L (600 mg/dL), and a resulting serum osmolarity that is greater than 320 mOsm. This leads to excessive urination (more specifically an osmotic diuresis), which, in turn, leads to volume depletion and hemoconcentration that causes a further increase in blood glucose level. Ketosis is absent because the presence of some insulin inhibits hormone-sensitive lipase mediated fat tissue breakdown.

Diagnosis[edit source]

Criteria[edit source]

According to the consensus statement published by the American Diabetes Association, diagnostic features of HHS may include the following:[6][7]

·       Plasma glucose level >30 mmol/L (>600 mg/dL)

·       Serum osmolality >320 mOsm/kg

·       Profound dehydration, up to an average of 9L (and therefore substantial thirst (polydipsia))

·       Serum pH > 7.4

·       Bicarbonate >15 mEq/L

·       Small ketonuria (~+ on dipstick) and absent-to-low ketonemia (<3 mmol/L)

·       Some alteration in consciousness

·       BUN > 30 mg/dL (increased)

·       Creatinine > 1.5 mg/dL (increased)

Imaging[edit source]

Cranial imaging is not used for diagnosis of this condition. However, if MRI is performed, it may show cortical restricted diffusion with unusual characteristics of reversible T2 hypointensity in the subcortical white matter.[8]

Differential diagnosis[edit source]

The major differential diagnosis is diabetic ketoacidosis (DKA). In contrast to DKA, serum glucose levels in HHS are extremely high, usually greater than 600 mg/dL (40-50 mmol/L), but an anion-gap metabolic acidosis is absent or mild. A temporary state of confusion (delirium) is also more common in HHS than DKA. Although traditionally DKA has been associated with Type I Diabetes, whereas HHS has been associated with Type II, HHS can be seen in people of both types. HHS also tends to have an elderly preponderance.

Symptoms similarities/differences

DKA involves a serum glucose level greater than 300 mg/dL. It usually occurs in type 1 diabetics whereas HHS is more common in type 2 diabetics. DKA is characterized by a rapid onset, and HHS occurs gradually over a few days. DKA also is characterized by ketosis due to the breakdown of fat for energy.

Both DKA and HHS may show symptoms of dehydration, polydipsia (extreme thirst), polyuria (excessive urination), polyphagia (extreme hunger), weight loss, nausea/vomiting/abdominal pain, blurred vision, headaches, weakness, and orthostatic hypotension.

However, symptoms unique to DKA include fruity breath (due to ketone bodies collecting in blood), kussmaul respirations (rapid and deep), and metabolic acidosis. Symptoms unique to HHS include seizures, myoclonic jerking, and reversible paralysis.

Management[edit source]

Intravenous fluids[edit source]

Treatment of HHS begins with reestablishing tissue perfusion using intravenous fluids. People with HHS can be dehydrated by 8 to 12 liters. Attempts to correct this usually take place over 24 hours with initial rates of normal saline often in the range of 1 L/h for the first few hours or until the condition stabilizes.[9]

Insulin[edit source]

Insulin is given to reduce blood glucose concentration; however, as it also causes the movement of potassium into cells, serum potassium levels must be sufficiently high or dangerously low blood potassium levels may result. Once potassium levels have been verified to be greater than 3.3 mEq/l, then an insulin infusion of 0.1 units/kg/hr is started.[11] The goal for resolution is a serum blood glucose of less than 200 mg/dL.

Electrolyte replacement[edit source]

Potassium levels will initially be high, but they lower as insulin therapy begins. Potassium levels usually range around 350 mEq in a 70 kg (154 lbs) person. Potassium should be administered with the IV replacement fluids. It is generally replaced at a rate 10 mEq per hour as long as there is adequate urinary output.[10]