Extra tips

Danielle B
By Danielle B Latest Reply 2010-06-01 12:21:43 -0500
Started 2010-05-26 13:37:18 -0500

Modifying Regular Recipes

Some cooks have tried and true recipes they enjoy so much
they find ways to make them so they're lower in fats and
calories — but just as tasty as ever. Here are a few of
their fat-lowering tricks:

- Cut the amount of fat in a recipe to half or less. This
won't drastically change the taste of most dishes.

- Use fat-free chicken broth rather than butter or oil to
sauté.

- Use skim milk, buttermilk, or even evaporated skim milk
in place of whole milk.

- Use 2 teaspoons of olive oil and a bouillon cube to
season your green beans rather than a ham bone.

You can actually have fun in serving your guests these
revised recipes and judging their reaction after you tell
them about their wonderful calorie and fat savings.

Danielle :)


13 replies

SkipT
SkipT 2010-05-26 21:23:26 -0500 Report

Here I go jumping on my "Fat is NOT the enemy" bandwagon. There is never been any study that shows that fat consumption causes the health problems we have been taught that it does. It has been shown that fat consumption along with carbohydrate consumption is what causes the problem. I cook full fat. Fry foods in rendered pork fat. I eat only regular foods, no low fat or fat free anything. My numbers don't lie. My cholesterol is 172. My triglycerides are 39! That is no typo, triglyceries are only 39. My coronary risk factor is 3.8 which is far below the average of 5.5.

Danielle B
Danielle B 2010-05-27 13:22:26 -0500 Report

Hi Skip T,

The numbers for you may be ok ( you want them below 200) but there is also the factor of heredity that may be on your side more than how and what you eat. My numbers are 135 for cholesterol and I eat baked or broiled everything (almost). I do not buy a lot of specialty foods because I know how to cook regular foods and you may want to check out a few medical journals on the studies factor. I did a study on cholesterol and the Beneficial butter in on e of my classes during my nutrition degree and the butter had stantons in it and thre was a significant differnece in the class' cholesterol levels at the end. I am in a family that is known heavily for high cholesterol and heart problems so me not being on any meds and my numbers being so good are due to how exercise and healthier eating effects my health. And YES the pork fat is going to hurt you in the end. What is your good cholesterol levels (LDL)? Mine is 67 and it needs to be above 35. That is increased or improved by eating things that contain Omeaga-3 fatty acids (nuts, peanutbutter, vitamins -under doctor's orders only!) and exercise (even just a walk). Try making a few adjustments before it is too late and you are on meds and a special diet that sounds like you would not want to floow very well with your current eating habits.

Words for thought!

Danielle :)

SkipT
SkipT 2010-05-27 16:41:05 -0500 Report

Actually it is through this very way of eating that I have been able to take myself off of my diabetes meds (metformin and actos). My pulse rate has dropped from a resting rate of 89 to a resting rate of 70. Blood pressure is 120/72. My good cholesterol (HDL) was 47. All kidney and liver functions are normal. I lost over 70 lbs and have kept the weight off for over 3 years. And since you mentioned statins for lowering cholesterol please read this:

Statin Side Effects
Statin side effects have been the subject of much controversy over the past few decades, as more and more research is revealing serious potential adverse reactions from statin medications. For this reason, many people seek natural cholesterol lowering alternatives to avoid statin side effects.

What are statin medications and how do they lower cholesterol?
Statin medications are prescription drugs that lower LDL (bad) cholesterol levels. Some of the more popular ones are Lipitor, Pravachol, Zocor and Mevacor. Some doctors recommend statin drugs even for patients who don't have high cholesterol as a precaution.

Liptor and other statin drugs work by blocking the enzyme that your liver needs to produce cholesterol. Although statins have no effect on HDL (good) cholesterol, they do succeed in lowering your LDL cholesterol. However, statins side effects can be very serious, and doctors should be more cautious when prescribing them for their patients.

What are statin side effects?
In addition to the common side effects such as headaches, nausea and fever, other statin side effects can be much more serious.

FACT: An FDA approved statin called Baycol was recently pulled off the market due to serious side effects and even deaths.

Two of the most troubling statin side effects include extreme muscle pain and muscle disease (statin induced myopathy), and serious liver problems.

According to an article in USA Today, a consumer watchdog group known as Public Citizen linked "72 fatal and 772 non-fatal cases of muscle breakdown (rhabdomyolysis) to all six of the statins sold between October 1997 and December 2000." Their research also revealed 29 earlier deaths.

Because of its effects on liver enzymes, statin side effects may include liver problems. Therefore, anyone with liver disease or prior liver issues probably should not take statin medications, and all of the statin manufacturers warn against it.

Other potential statin side effects:

Although muscle pain and statins and liver problems are of the most concern, much research has shown that statin side effects could include sexual dysfunction and performance problems, as well as memory loss, personality changes and irritability.

Other concerns regarding prescription cholesterol lowering drugs:
1) While cholesterol lowering drugs do lower LDL (bad) cholesterol, they have limited effect on HDL (good) cholesterol, and no effect on triglycerides (fats), an equally important heart disease risk indicator.

2) Statin medications decrease your body's supply of CoEnzyme Q10 (CoQ10), which is an essential nutrient for heart strength and function.

Danielle B
Danielle B 2010-05-30 20:06:58 -0500 Report

Hey,

You havelost all that weight becuase you deprived your body of energy providers and so it had to burn up the fat and muscle it needed to survive. I leave the stanton debate to the dr and hte pharmacists that deal with the individual patient's issues. Have you checked your keytones lately? You do know that burning all that fat and not eating carbs is the best way to develop ketoacidosis? That was the major concern with the Atkin's Diet. AGAIN that 4-letter word…DIET!

Danielle :)

SkipT
SkipT 2010-05-31 05:25:02 -0500 Report

No enegy loss here. I walk 3 miles a day. I lift weight 3 times a week, I do wind sprints twice a month, and I have a job where I sometimes lift a total of over 2000 lbs a day in 150lb increments. I am 62 years old and out work guys who are half my age. I don't have a diet, I have a lifestyle that works. Keytones are fine by the way, as ketoacidosis is a problem with people who already have kidney issues. You know that the body doesn't need to consume any carbs at all. The process is called neoglucogenesis.

Danielle B
Danielle B 2010-05-31 16:02:19 -0500 Report

There are different sttrokes for different folks! I highly suggest that if anyone reading this discussion is interested in learning more about anything said that you 1) check with your dr, 2) know your own body's linits and start slow, and read info at end on everything about ketoacidosis: very long so choose what you want to know but it is out of a reputable medical journal. Will add info at end of this message!

The truth about the kidneys beinga pre-conditioned problem before you develop ketoacidosis is not true. A normally healthy diabetic that suddenly turns sick can develop this problem and require medical treatment. But YES, it does involve the kidneys once it is an issue.

Here is info. BEWARE there is a lot of it and there are a lot of technical terminology that you may want to discuss with CDE or endo dr first.

Description

Life-threatening complication of diabetes mellitus
Requires urgent inpatient treatment
Severe electrolyte imbalance with dehydration
Severe insulin shortage
May be the initial presenting feature of diabetes mellitus
Mainly occurs in patients with type 1 diabetes mellitus but can occur in patients with type 2 diabetes mellitus
Look for underlying infections and other precipitating factors

Synonyms

DKA
Diabetic ketosis
Diabetic acidosis

Immediate action

Admit the patient to the hospital intensive care unit (ICU) for correction of insulin shortage and electrolyte imbalance, rehydration, and treatment of precipitating factors.

Background

Cardinal features

Dehydration with polyuria, polydipsia, polyphagia
Acetone ('fruity') breath odor
Kussmaul (sighing) respiration
Abdominal pain
Altered consciousness
Nausea/vomiting
Shock—tachycardia, hypotension
Underlying diabetes mellitus in all cases
May be the initial presentation of diabetes mellitus, especially in children
Most commonly occurs in patients with type 1 diabetes mellitus
Can occur in patients with type 2 diabetes mellitus
Requires urgent rehydration, insulin replacement, and correction of electrolyte imbalance

Causes

Common causes

Diabetes mellitus is the only underlying cause of diabetic ketoacidosis (DKA). The pathogenesis of DKA involves insulin deficiency and increased production of catabolic hormones (glucagon, cortisol, catecholamines, and growth hormone). Insulin deficiency can either consist of a complete lack of insulin production or a relative deficiency of insulin given the patient's physiologic needs. These changes result in hyperglycemia (by decreasing peripheral utilization of glucose and increasing hepatic production of glucose) and ketosis through production of ketoacids as an alternative energy source.

Hyperglycemia induces profound osmotic diuresis, causing water and electrolyte loss, especially potassium
Ketosis causes metabolic acidosis
Metabolic acidosis forces hydrogen ions into cells, displacing potassium ions that are lost through urine and vomiting
Total-body potassium depletion is present, but serum potassium levels may be normal or high because of electrolyte shift
Extreme fluid loss results in clinical shock
In some cases, hyperglycemia and dehydration predominate, and acidosis is minimal
Undiagnosed diabetes mellitus may present acutely because of pancreatic islet cell destruction resulting in lack of insulin production
Type 1 diabetes mellitus:

Two thirds of patients hospitalized for DKA have type 1 diabetes
Undiagnosed diabetes mellitus may present acutely due to pancreatic islet cell destruction, resulting in lack of insulin production
Islet cell destruction is usually autoimmune, possibly with a viral trigger (especially in children); rarely, it may be secondary to pancreatic destruction (eg, chronic pancreatitis, pancreatic cancer)
Life-long insulin therapy is required
Insulin requirements in children may increase dramatically at the onset of puberty
Type 2 diabetes mellitus:

One third of patients hospitalized for DKA have type 2 diabetes
Clinical presentation is similar to that of classic type 1 DKA
Most often related to conditions of severe physical stress (life-threatening infection, trauma, acute cardiovascular disease)
Increased incidence of DKA without an associated precipitating cause has been reported in black and Hispanic persons; over half of these individuals have newly diagnosed type 2 diabetes and are classified as having ketosis-prone type 2 diabetes mellitus
Often after a short course of insulin therapy, discontinuation of insulin is possible, and glycemic control can be maintained with diet and oral medications alone

Contributory or predisposing factors

Most cases of DKA have a precipitating event. A thorough investigation for precipitating events is imperative to ensure appropriate management.

Pre-existing diabetes mellitus (diagnosed or undiagnosed)
Infection, including urinary tract infection, viral gastroenteritis, pneumonia, and other foci of sepsis (eg, poor periodontal hygiene and dental caries)
Noncompliance with medication regimen and/or diet
Severe medical illness (eg, myocardial infarction, cerebrovascular event)
Trauma or surgery
Severe psychological distress
Pregnancy
Cocaine abuse has been reported as a risk factor for recurrent DKA
Chaotic lifestyle
Bulimia in adults or adolescents, dieting, and unhealthy eating patterns
Use of medications that affect carbohydrate metabolism (eg, glucocorticoids, high-dose thiazides, antipsychotics, sympathomimetics)
Consider Munchausen's syndrome in adults and Munchausen's syndrome by proxy in children
Consider child physical abuse and neglect
Idiopathic

Epidemiology

Prevalence

In the landmark Diabetes Control and Complications Trial, the rate of DKA in adults on the conventional insulin protocol was 1.8 per 100 person-years compared to a rate of 2.0 per 100 person-years in those on an intensive insulin protocol
DKA is a common finding at the time of diabetes presentation, occurring in 29% of patients with type 1 diabetes and 10% of patients with type 2 diabetes
From 1985 to 2005, there was a 42% increase in the number of hospitalizations for DKA

Mortality

Overall mortality rate for adults is less than 1%
Mortality rate in the elderly and in patients with significant comorbidities is greater than 5%
Most common cause of death in children and adolescents with type 1 diabetes

Economic impact

Results in more than 500,000 hospital days per year in the U.S.
Direct and indirect cost of 2.4 billion U.S. dollars annually

Demographics

Age

Of patients hospitalized for DKA:

18% are under age 20
56% are aged 18 to 44 years
24% are aged 45 to 65 years

Race

Slightly more predominant in whites (45% nonwhite).

Codes

ICD-9 code

250.10 Diabetes with ketoacidosis, type II or unspecified type, not stated as uncontrolled
250.11 Diabetes with ketoacidosis, type I [juvenile type], not stated as uncontrolled
250.12 Diabetes with ketoacidosis, type II or unspecified type, uncontrolled
250.13 Diabetes with ketoacidosis, type I [juvenile type], uncontrolled
250.30 Diabetes with other coma, type II or unspecified type, not stated as uncontrolled

Diagnosis

Clinical presentation

Symptoms

Polyuria
Thirst
Weight loss despite increased appetite
Weakness
Nausea
Vomiting—may be biliary
Abdominal pain
Muscle cramps
Blurred vision
Pyrexia
May be a recent history of:

Increased appetite (polyphagia)
Weight loss
General malaise, lethargy
Increased susceptibility to minor infection (eg, paronychia)
Poor wound healing

Signs

Dehydration:

Sunken eyes
Hypotension
Tachycardia
Reduced skin turgor
Bradycardia when shock is extreme and decompensation occurs
Hypothermia
Confusion, altered consciousness
Weight loss
Poor tissue perfusion (prolonged capillary reaction time in children)
Metabolic acidosis:

Air hunger (Kussmaul breathing)
Acetone ('fruity') breath odor
Examples of precipitating event:

Pneumonia
Wound infection

Associated disorders

Remember to look for a precipitating event; consider occult sepsis.

Differential diagnosis

Hyperglycemia without acidosis

Not acutely dangerous if the patient is healthy
Increases the short-term risk of infection and, hence, the risk of developing DKA
Prolonged periods of hyperglycemia increase the long-term complication rate

Features

Elevated blood glucose level
No ketonuria
Normal plasma pH (>7.3)
Normal serum bicarbonate level

Nonketotic hyperosmolar coma

Usually affects elderly patients, many of whom have previously undiagnosed type 2 diabetes mellitus
Level of consciousness is depressed when plasma osmolality is high
May be precipitated by concomitant use of certain quinolone antibiotics in patients with diabetes taking certain oral hypoglycemic agents

Features

Severe hyperglycemia (>600 mg/dL)
No significant ketonuria/ketonemia
No significant acidosis
Usually occurs in elderly patients
Markedly elevated plasma osmolality
Thromboembolic complications are common
Insulin requirement is less than that for DKA
Requires ICU monitoring

Alcoholic ketoacidosis

Acute alcoholic binge in the setting of poor dietary intake.

Features

High serum ketone levels; predominant ketone body is β-hydroxybutyrate
Elevated anion gap
Dehydration with elevated blood urea nitrogen (BUN) and creatinine is common
Blood glucose levels can range from low to slightly elevated; blood glucose level is rarely >200 mg/dL (blood glucose is markedly elevated in patients with DKA)
Often accompanied by nausea, vomiting, and abdominal pain
Precipitating factor is common (pancreatitis or infection)
Measurement of glycosylated hemoglobin can help evaluate for chronic hyperglycemia

Starvation ketoacidosis

Hepatic glycogen stores become exhausted after 12 to 24 hours of fasting; ketogenesis by the liver occurs to provide energy for peripheral tissues.

Features

Mild ketosis can occur with low-carbohydrate diets (eg, Atkins diet)
Ketoacid levels typically do not exceed 10 mEq/L
Blood glucose level is not elevated

Lactic acidosis

Most common cause of metabolic acidosis in hospitalized patients
Can occur concomitantly with DKA
Patient is likely to be taking a biguanide in the setting of impaired renal function
High mortality rate (>50%)

Features

Overbreathing
Dehydration is not as severe as that typical of DKA coma
No acetone breath odor
Mild or no ketonuria
Low pH (200 mg/dL) and creatinine (>10 mg/dL) and no hyperglycemia.

Features

pH and anion gap are only slightly abnormal
Requires supportive treatment; dialysis may be necessary
Evaluate for rhabdomyolysis as a cause (elevated serum concentrations of myoglobin and creatinine phosphokinase)

Salicylate toxicity

Incidence has decreased in recent years.

Features

Nausea, vomiting
Tinnitus
Sweating
Vasodilation
Hyperventilation, especially in children
Impairment of consciousness, confusion, stupor, coma
Metabolic acidosis predominates in children
Respiratory alkalosis predominates in adults
Elevated plasma salicylate levels

Ethylene glycol/methanol poisoning

Or other organic alcohols that cause anion gap acidosis.

Features

Inebriation
Hyperventilation
Altered consciousness
Convulsions
Increasing acidosis and severe anion gap

Poisoning—other common substances

History is important but may not be available due to loss of consciousness.

Features

Dependent on the substance ingested; may include:

Altered consciousness
Vomiting
Diarrhea
Gastrointestinal hemorrhage
Bradycardia
Tachycardia
Hypotension
Metabolic acidosis
In particular, iron toxicity may cause shock, coma, and acidosis

Diabetes insipidus

Diabetes insipidus is an uncommon differential diagnosis.

Features

Polyuria
Polydipsia
Patient may be able to maintain an adequate fluid balance; if not, dehydration may occur rapidly

Urinary tract infection

Urinary tract infection may present with nonspecific symptoms in children and elderly patients.

Features

Urinary frequency
Urinary urgency
Dysuria
Abdominal pain
Flank pain
Pyrexia
Vomiting

Workup

Diagnostic decision

DKA is not an absolute diagnosis
DKA is a medical emergency requiring admission to the ICU for close monitoring and treatment
Suspect DKA in patients with significant ketosis, hyperglycemia, and clinical dehydration
A commonly used definition of DKA is pH 250 mg/dL but generally not >800 mg/dL, and is essential for monitoring progress. May be obtained by the primary care physician with a glucometer to aid in initial diagnosis, but a serum glucose level should also be obtained from the laboratory to confirm the diagnosis
Urine/serum ketones: Measurement of ketones is essential in any patient with diabetes who is unwell. Moderate to high ketone levels suggest DKA in an ill patient with diabetes and elevated blood glucose
Arterial blood gas analysis: reveals acidosis and bicarbonate level; allows assessment of severity and monitoring of progress. Typically, pH is 126 mg/dL (although in most cases the level will be >250 mg/dL) in the presence of illness and ketonuria suggests DKA.

Cause of abnormal result

DKA if the patient is unwell
Also consider hyperglycemic nonketotic states
If the patient is well and not ketotic, elevated glucose levels may indicate poor glycemic control or a recent meal or sugary drink

Medications, disorders, and other factors that may alter results

Recent consumption of a large meal will cause an elevation in blood glucose in a patient who is well
Recent consumption of a glucose-containing treat or drink will also boost blood glucose initially
In patients without diabetes, postprandial glucose should not increase above 200 mg/dL, and ketones should only be present in the urine if the patient has not eaten, is dehydrated, or is in a catabolic state (eg, DKA)
Ten percent of patients with DKA will present with a blood glucose level 7.3 is not consistent with DKA, unless a second or third acid-base derangement is present

Abnormal

In patients with DKA, the pH at presentation is 10 to 12 mEq/L are indicative of increased anion gap metabolic acidosis

Cause of abnormal result

Serum sodium:

Hyperglycemia produces an osmotic effect, leading to movement of extravascular water to the intravascular space. As hyperglycemia resolves, serum sodium levels normalize
Serum potassium:

Increased loss of potassium in the urine due to glucose-driven osmotic diuresis and the excretion of ketoacids lead to total-body potassium depletion
Gastrointestinal losses may also contribute to deficiency
Once treatment with insulin has begun, unless potassium is repleted, life-threatening hypokalemia can ensue
Serum bicarbonate:

Acidosis is due to production and accumulation of ketones in the serum

Medications, disorders, and other factors that may alter results

If a patient with uncontrolled diabetes also has significant hyperlipidemia, the serum will be lactescent (milky appearance due to a high concentration of lipids); this can lead to pseudohyponatremia. The use of ion-selective electrodes in the measurement of electrolytes has made this less of a concern
Serum sodium, potassium, and/or bicarbonate abnormalities in the absence of hyperglycemia, acidosis, and ketosis require further investigation, as such abnormalities are not likely due to DKA

Serum phosphate, calcium, and magnesium

Description

Patients with DKA generally have total-body phosphate depletion. However, the serum phosphate level does not reflect this and is usually either normal or, occasionally, high
Serum calcium and magnesium also may be significantly reduced and may decrease further with treatment; thus, levels should be rechecked every few hours

Normal

Serum phosphate: 2.4 to 4.1 mg/dL
Serum calcium: 8.2 to 10.2 mg/dL
Serum magnesium: 1.3 to 2.1 mEq/L

Abnormal

Values outside of the normal ranges.

Cause of abnormal result

Serum phosphate:

Decreased phosphate intake
Renal phosphate wasting due to osmotic diuresis
Serum calcium:

Decreased calcium or vitamin D intake
Renal disease
Disorders of bone metabolism
Hypocalcemia resulting from phosphate administration
Serum magnesium:

Decreased magnesium intake or malabsorption
Alcoholism
Diuretic use

BUN and creatinine

Description

Assessment of renal function
Renal function may be compromised at baseline due to underlying diabetic nephropathy
Dehydration can lead to impaired renal function
Estimated glomerular filtration rate (GFR) should also be assessed, as it takes into account patient-specific factors, such as gender, age, and race
The severity of acidosis in the setting of DKA is often minimized in patients with normal renal function because their kidneys are able to compensate by increasing renal acid excretion

Normal

BUN: 8 to 23 mg/dL
Creatinine: 0.6 to 1.2 mg/dL
Estimated GFR: 90 to 120 mL/min

Abnormal

Values outside of the normal range
Estimated GFR 25,000/µL or a band percentage in excess of 10 should prompt evaluation for infection, including blood and urine cultures as well as culture of any other accessible body fluid

Cause of abnormal result

Leukocytosis occurring in patients with DKA that is unrelated to infection is thought to be due to hypercortisolemia and sympathetic activation due to physiologic stress.

Blood cultures

Description

Obtain in patients presenting with DKA who have significant leukocytosis, fever, or other clinical findings suggestive of systemic infection.

Normal

No bacterial growth.

Abnormal

Bacterial growth.

Cause of abnormal result

Bacterial infection in the bloodstream, which may be a precipitating cause for DKA.

Urinalysis

Description

Obtain a clean-catch midstream specimen if possible
Used to monitor for ketones, as described under Urine/serum ketones
Dipstick is also likely to show moderate to high glucose levels, confirming hyperglycemic state in the absence of a glucometer
Can be used to assess for infection within the genitourinary tract, which may be a precipitating factor for DKA
Do not delay hospital admission if the patient is unable to pass urine

Normal

No evidence of infection, blood, or other abnormality.

Abnormal

In a patient with diabetes, even trace levels of ketones are of concern
Positive leukocyte esterase and nitrite test results and a leukocyte count >5/high-power field are suggestive of a urinary tract infection, and, at minimum, a urine culture for sensitivity should be obtained

Cause of abnormal result

DKA
Not eating—catabolic state (eg, excessive dieting, hyperemesis gravidarum)
Infection

Medications, disorders, and other factors that may alter results

Any state in which the patient has not eaten for some time due to intercurrent illness or excessive dieting (eg, anorexia nervosa); however, hyperglycemia is not usually a feature of these conditions
Results from expired urine dipsticks cannot be trusted

Imaging

Chest radiograph

Description

Can be used to assess for pulmonary infection as an inciting event for DKA
Should be obtained during the initial workup

Advantages/disadvantages

Advantages:

Readily available and noninvasive
Can usually establish the diagnosis of pneumonia and other pulmonary infections

Normal

A classic view of the chest cavity.

Abnormal

Infiltrative process suggestive of pneumonia.

Cause of abnormal result

Pneumonia
Other pulmonary infections

Other tests

Electrocardiography

Description

Appropriate if transfer times to the hospital are prolonged and the primary care physician is accompanying the patient
May be used to determine whether to add intravenous potassium chloride to the rehydrating solution during prolonged transit with the physician accompanying the patient. Potassium should only be added to intravenous fluids once the patient is urinating

Advantages/disadvantages

Advantages:

Noninvasive
Relatively inexpensive

Abnormal

Tall, narrow, or tent-shaped T waves; decreased or absent P waves; short QT intervals; widening of QRS complex: indicative of hyperkalemia
Flattening of T waves, U waves present in most leads: indicative of hypokalemia
Intravenous potassium administration is potentially dangerous, so in the absence of biochemical monitoring, it is necessary to be sure that hyperkalemia is not present. If certain there is no evidence of hyperkalemia, potassium chloride, 20 to 40mEq/L, may be added to the rehydrating solution

Clinical pearls

DKA is often precipitated in patient known to have diabetes who has decreased or discontinued insulin in the face of decreased oral intake (eg, during a vomiting illness). It is important to counsel patients with diabetes that insulin is always required by the body and that discontinuing insulin is an incorrect response to illness. Patients should make adjustments to their insulin doses in conjunction with their physician when they are experiencing an intercurrent illness
It is always worthwhile to do a fingerstick to check random blood glucose levels in patients who present with general malaise and weight loss

Consider consult

Consider consulting an endocrinologist for further assistance.

Treatment

Goals

Refer urgently for lifesaving treatment
Increase the rate of glucose utilization by insulin-dependent tissues
Reverse ketonemia and acidosis
Correct fluid and electrolyte depletion
Avoid iatrogenic cerebral edema
Encourage the patient to seek medical care earlier if similar symptoms begin again
Discover the cause of the episode in order to prevent future occurrences of DKA
Reassess the patient after the acute episode, and seek to improve the patient's understanding and management of diabetes

Immediate action

Normally, the role of the primary care physician is to arrange immediate and rapid transfer to a hospital and not to initiate treatment, which is unsafe and difficult to titrate without close biochemical monitoring
In remote areas where transfer times to units able to monitor acid and electrolyte balance are significant, fluid and insulin replacement may be cautiously commenced in transit. Careful monitoring for fluid overload is essential. Physicians should be very familiar with the management of patients with DKA because there is a significant risk of rapid electrolyte shifts and cerebral edema if fluids and insulin are administered too rapidly
Initial fluid replacement should be with 0.9% normal saline. The fluid replacement rate varies depending on the patient's age and whether significant cardiac or renal disease is present
In adults:
The usual rate of fluid infusion is 500 to 1,000 mL in the first hour followed by 300 to 500 mL/h until arrival at the hospital. Err on the side of caution if in doubt
Traditionally, the insulin infusion rate is a bolus loading dose of 0.1 U/kg followed by a constant infusion of 0.1 U/kg/h until arrival at the hospital. However, recent data suggest that a priming bolus dose is not required if the initial infusion rate is 0.14 U/kg/h
If continuous intravenous insulin administration is not possible, subcutaneous or intramuscular administration of a short-acting or rapid-acting insulin analog (eg, insulin lispro or insulin aspart) every 1 to 2 hours is safe and may be as effective as intravenous insulin. Administer an initial subcutaneous dose of 0.3 U/kg followed by 0.1 U/kg every hour until the serum glucose level is 5.5 mEq/L
Because phosphorus may also be depleted in patients with DKA, consider using half potassium chloride and half potassium phosphate initially for potassium replacement

Dose

The average potassium loss in adults is 500 to 700 mEq
Rate of replacement varies with the patient's serum potassium level
In patients with normal renal function: add 20 to 40 mEq/L
In children: after initial fluid resuscitation, review urine and electrocardiographic findings, and add potassium chloride, 20 to 40 mEq/L

Contraindications

Severe renal impairment
Sodium polystyrene sulfonate
Hyperkalemia
Oliguria, anuria, azotemia
Severe hemolytic reactions

Cautions

Use caution in elderly patients and in patients with renal disease or impairment, adrenal insufficiency, cardiac arrhythmias, acute dehydration or diarrhea, severe burns, or heat or muscle cramps.

Monitor

Serum potassium
BUN and creatinine

Adverse effects

Hyperkalemia, electrocardiographic changes, arrhythmias, hypotension, atrioventricular block, cardiac arrest, paresthesias, confusion, shock, nausea, vomiting, abdominal pain, diarrhea, gastrointestinal bleeding, esophageal/small bowel ulceration, weakness.

Interactions

Amphotericin B (increased risk of developing hyperkalemia)
Angiotensin-converting enzyme inhibitors (may increase serum potassium levels)
Angiotensin II receptor antagonists (may increase serum potassium levels)
Antimuscarinics (may increase the risk of gastrointestinal irritation)
β-Blockers (increased risk of developing hyperkalemia)
Cyclosporine (may increase serum potassium levels)
Diuretics, including potassium sparing (may increase serum potassium levels), loop, and thiazide (increased risk of developing hyperkalemia)
Eplerenone (may increase serum potassium levels)
Heparin (may increase serum potassium levels)
Loperamide (may increase the risk of gastrointestinal irritation)
Penicillins (may increase serum potassium levels)
Sodium polystyrene sulfonate (avoid concomitant use)
Trimethoprim (may increase serum potassium levels)

Pregnancy and lactation

Use during pregnancy when the potential benefit to the mother justifies the risk to the fetus; monitor serum potassium levels
Effect on potassium content of breast milk is unknown but is not believed to be significant; monitor serum potassium levels in breast-feeding women

Pregnancy category

Pregnancy category C.

Cefotaxime

If an underlying infection is suspected, which is often the case, administer a broad-spectrum intravenous antibiotic (eg, a third- or fourth-generation cephalosporin) while awaiting the results of blood cultures.

Dose and dose information

Adult

Intravenous: 2 g every 4 to 6 hours, not to exceed 12 g/d.

Pediatric

Intravenous: 50 to 200 mg/kg given in 4 to 6 equally divided doses.

Hepatic/renal impairment

Use caution in patients renal impairment; a dose reduction may be necessary.

Efficacy

Active against gram-positive and gram-negative organisms and anaerobes.

Contraindications

Cephalosporin hypersensitivity.

Cautions

Risk of cross-sensitivity with penicillins. Use extreme caution in patients with a history of penicillin hypersensitivity
Risk of pseudomembranous colitis. Use caution in patients with gastrointestinal disease, particularly colitis
Risk of granulocytopenia and, more rarely, agranulocytosis, particularly with prolonged therapy
Potentially life-threatening arrhythmias following rapid (

Danielle B
Danielle B 2010-06-01 12:21:43 -0500 Report

So is breathing but there are people that have trouble with that too and are under medical advuce. I still suggest anyone to talk to a dr first!

Emma2412
Emma2412 2010-05-31 17:35:25 -0500 Report

No, Danielle, that diet doesn't cause ketoacidosis and it doesn't do anything bad to one's kidneys, either. That's been medically proven.

Emma2412
Emma2412 2010-05-31 17:33:51 -0500 Report

Hey, again, Skip
Hurrah for you for mentioning the statin side effects and the damage those drugs can do!! Why anyone would want to submit themselves to taking something like that is beyond me. Don't people read up on the side effects of a medicine before they submit to taking it? I know I do. Only then do I make an informed decision as to whether I should or should not take it. I've already told my doctor that I refuse to take any kind of statin. She was mad at first, but now she's working with me. The first thing I'm trying is niacin, the flughless kind. If that doesn't work, then she'll tell me something else to try.
As to diabetic meds, I figure until I can come up with a plan that will work for me, I'll take them simply to lower the risk of diabetic complications, but once I figure it out for my body (and I think I'm almost there), I'm going to get them out of my life, believe me. Why? I hate drugs of all description.
Now, I also just want to say that I don't know why there are people out there who just accept whatever doctors prescribe for them without first doing some research into what that drug or drugs can do to them. The information is out there, like I said. You can do your research and then call the doctor and tell him your decision. Don't just accept it without question. It's your body, not the doctor's body.
Remember back in the '70's the government was telling us all — and doctors went along with it — that a no-fat diet was the only way to go. They drilled that into people's heads. But what happened? We had a diabetes epidemic.
So, don't just accept the politically-correct-at-the- moment medical hype. The problem with the medical profession and the government is that they come out with things before they've been definitely proven and people jump at it. The fact that they come out with something before the research is complete is really criminal. Oh, people, I got to go. I think I want to call my lawyer.

Emma2412
Emma2412 2010-05-31 17:06:41 -0500 Report

Hi, Skip
I tried the Atkins Diet about 15 years ago. I was not diabetic at that time, just overweight about 20 pounds. The weight came right off and I felt great. However, about 10 years ago, I had gained that 20 pounds back, plus a few.
There is a theory that it's a combination of saturated fat and the wrong kinds of carbs that creates the problem and I believe that's basically what Atkins said in his book years ago after he formulated his diet plan. But there must be something to it just from my own experience with the Atkins Diet, and also with the fact that Atkins reported people having wonderful cholesterol levels, etc., etc.
Since I'm having trouble with my cholesterol levels, I'm seriously thinking of trying the Atkins Diet again. But I would never cook in rendered pork fat. I'll use olive oil instead.
Ihave a good friend who is a podiatrist who recommended the South Beach Diet to me. The SB Diet was formulated by a cardiologist who was looking for a way to help his patients with their heart problems.
From a health standpoint, I think what the AMA and others are now looking for is the effect so much saturated fat will have on the whole body over a period of years, especially as a person gets older.
I, too, am a fan of regular food. I hate margarine, for instance, and never buy it nor do I buy anything that's marked "low-fat" or "no-fat". It's junk food, in my opinion, loaded with sugars, salt and chemicals that they use to try and make the product taste "normal."
You know, I do wonder why there's all this hype about sugar substitutes and the chemicals that are in them, but I never hear anybody talk about the chemicals that they put in a low-fat or no-fat cheese, for instance.
But I can tell you one thing, Skip. I wish I had your numbers!

petals
petals 2010-05-26 14:16:39 -0500 Report

I use alot of the tips that you have here. I didn't know about the green bean one thank you.