Diabetes and glycemic emergencies

Glycemic items turn on one decision: is the brain getting glucose right now, or is the client drowning in sugar and acid? Name that first, then pick the sequence.

Hypoglycemia vs hyperglycemia

The brain runs on glucose. When the level drops, adrenergic and neuroglycopenic signs appear first. Shake, sweat, hunger, then confusion and seizure risk. Because neurons are starving. High glucose pulls water into the urine (osmotic diuresis), so the client looks dry and thirsty, not hypoglycemic. Name which problem you are in before you reach for insulin or sugar.

• If the client is unresponsive, do not force oral sugar. Airway and parenteral rescue first.
• After a hypo is corrected, follow with a snack that holds the glucose (protein + complex carb) unless the next meal is imminent.

Bedside order for hypo: can they protect their airway and swallow? If yes, fast-acting carbohydrate now. If no, glucagon or IV dextrose per protocol. Juice in an unprotected airway causes aspiration. Once the acute low is corrected, a protein-plus-complex-carb snack holds the level until the next meal; a pure sugar bounce without follow-up often rebounds into another low.

The distractor that looks tidy is giving scheduled insulin because the chart says hyperglycemia, or forcing oral sugar into a confused, seizing, or unresponsive client. Treat the life threat in front of you: critically low glucose before insulin; airway before oral carbs. Hyperglycemia without airway compromise is a fluids-and-driver problem, not a candy rescue.

DKA vs HHS

Both are volume emergencies from relative or absolute insulin lack, but the chemistry differs. In DKA, fat breakdown floods the blood with ketones and an anion-gap metabolic acidosis. That is why you see Kussmaul breathing (blowing off CO₂) and fruity breath. In HHS, enough insulin usually remains to limit ketosis, so glucose climbs extremely high, osmolality soars, and dehydration is profound; mental status change tracks that dehydration more than acid.

Why fluids before the insulin drip in DKA: the client is intravascularly dry from osmotic diuresis. Insulin without volume correction worsens hypovolemia and can crash potassium as glucose and potassium shift into cells. Replace and monitor potassium per protocol around the drip. Serum K may look “normal” while total body potassium is already low. HHS still needs aggressive rehydration; glucose correction is gradual so osmolality does not swing too fast.

The distractor that looks protocol-smart is starting insulin first because “that is the diabetes drug,” or treating every high glucose the same way. Use the fork: ketones and acidosis point to DKA sequencing; extreme hyperglycemia with little or no ketosis and deep dehydration points to HHS. Edge case: a client on an insulin pump who stops receiving basal insulin can tip into DKA even without a classic “new type 1” story. Missing insulin is missing insulin.

Insulin timing (exam level)

You do not need every brand name. You need which class peaks when, because peak = hypo risk and meal timing.

Mixing (when ordered)

1. Clear before cloudy when drawing (rapid/regular, then NPH).
2. Do not mix long-acting glargine into the same syringe.
3. Verify dose with a second nurse when policy requires it for insulin.

Sick-day rules

Illness raises counter-regulatory hormones (cortisol, catecholamines, glucagon), so glucose climbs even when the client is eating less. That is why basal insulin usually continues: stopping it because “they are not eating” is how type 1 clients tip into DKA. More frequent checks catch the climb; ketone checks (when taught) catch the turn into fat metabolism before the client is critically acidotic.

• Keep taking basal insulin unless the provider says otherwise. Illness raises glucose.
• Check glucose (and ketones when taught) more often; hydrate.
• Call for persistent vomiting, ketones, or glucose that will not come down. That is DKA risk, not a wait-it-out day.

Bedside teaching: hydrate if oral intake is possible; keep basal coverage; escalate when vomiting prevents intake, ketones appear, or glucose will not respond to the sick-day plan. Persistent vomiting is not “wait until morning”. It is dehydration plus inability to take oral carbs or meds, which stacks DKA risk.

The distractor that sounds cautious is holding all insulin until the client eats normally again. Holding prandial doses when meals are skipped may be appropriate per plan; holding basal in type 1 without a provider order is the trap. Another false comfort: assuming “just a virus” needs only rest. If ketones or refractory hyperglycemia show up, treat it as an emergency pathway, not a tough-it-out day.

Injection sites, A1c, and daily control

Subcutaneous insulin lands in fat, not muscle. The abdomen usually absorbs most predictably; outer thigh, upper arm, and buttocks are rotation options. Stay about an inch from the umbilicus and never reuse a scarred or lumpy (lipohypertrophic) patch. That tissue absorbs erratically and creates unexplained highs and lows. Pinch technique and needle length follow the teaching plan; the exam trap is rotating through the same golf-ball of hypertrophy because “it hurts less.”

A1c (glycosylated hemoglobin) binds glucose to hemoglobin over the red cell’s life, so it reports months of average glycemia. Use it for “are we meeting the control goal” conversations. Do not use a single A1c to decide whether this minute’s confusion is hypo or DKA. Point-of-care glucose still drives the emergency fork.

Oral antidiabetic classes, metformin holds before contrast, and steroid-driven hyperglycemia live in Oral antidiabetics and corticosteroids. Keep this chapter on insulin timing, emergencies, and the lifestyle moves that prevent the next crisis.

Chronic complications and foot care

Years of hyperglycemia injure small vessels and nerves. Retinopathy threatens vision; nephropathy raises creatinine and urine protein; peripheral neuropathy dulls protective sensation so a pebble in the shoe becomes an ulcer, then infection, then amputation risk. Autonomic neuropathy can mask classic hypo warning signs and disturb gastric emptying. The nursing win is prevention teaching that the client can do every day, not a lecture after the wound is deep.

• Inspect feet daily (use a mirror or helper); report breaks, redness, or drainage early.
• Closed shoes that fit; no barefoot walking; careful nail care as taught (often podiatry if sensation is lost).
• Keep skin moisturized but dry between toes; avoid heating pads on numb feet.
• Annual eye exams and urine albumin/creatinine checks as ordered are disease control, not optional extras.

The distractor that looks practical is soaking numb feet in hot water, using a heating pad for “circulation,” or ignoring a small blister because it does not hurt. No pain is the danger when neuropathy is present. Another miss: treating retinopathy teaching as vanity when the real issue is preventable blindness with glycemic and BP control plus ophthalmology follow-up.

Exercise and the glucose swing

Muscle work usually increases glucose uptake, so activity can drop the level, especially around insulin peak. Check glucose before exercise; if already low or trending down, treat and delay. Carry fast carbs for unexpected lows. Long or intense sessions may need a snack per the plan. Illness and steroids raise glucose; exercise is not a substitute for sick-day insulin. The exam trap is sending a client with ketones out for a hard workout “to burn sugar”. Ketones mean stop and follow the illness pathway, not more stress hormones from exertion.

How to reason under time pressure

1. Is the client hypo right now? If yes, treat glucose delivery first.
2. If hyper with illness: fluids and the DKA/HHS fork (ketones/acidosis vs extreme dehydration).
3. Match insulin action to food and peak risk; never push oral carbs into an unprotected airway.
4. For chronic stems: feet, eyes, kidneys, and site rotation beat another lecture on pathophysiology alone.