Endocrine Disorders: Diabetes Mellitus

Diabetes is the disease you will meet on every unit you ever work, attached to every other diagnosis you have already studied — the heart failure patient, the post-op abdomen, the pneumonia, the pressure injury that will not close. It is also the disease in which nursing judgement is measured in minutes: a capillary glucose of 48 mg/dL, a patient breathing deeply and smelling faintly of acetone, an insulin drip running while the potassium is 3.1 mEq/L. This chapter builds the reasoning from the inside out. First the mechanism — why absent insulin produces ketones and why resistant insulin produces dehydration. Then the assessment and the numbers that define the disease. Then the drugs, organised by what they actually do, because that is what tells you when they cause hypoglycaemia and when they do not. Then the two hyperglycaemic emergencies side by side, with the treatment sequence you will be expected to defend: fluids first, potassium before insulin, insulin last. Then the slow complications and the teaching that prevents them.

Section 1Two Ways the Pancreas Fails

Insulin is the storage signal, and everything follows from that

Beta cells in the islets of Langerhans release insulin when blood glucose rises after a meal. Insulin does three things worth memorising because every sign of diabetes traces back to one of them. It opens GLUT4 transporters in muscle and adipose tissue so glucose leaves the blood and enters cells. It tells the liver to stop making new glucose — to suppress glycogenolysis and gluconeogenesis. And it suppresses lipolysis, keeping fatty acids locked inside adipocytes. Alpha cells in the same islet release glucagon, which does the opposite, and the fed-fasted balance between the two normally keeps plasma glucose in a remarkably narrow band of roughly 70 to 140 mg/dL across a whole day of eating and sleeping.

Remove insulin and all three brakes release at once. Glucose cannot enter muscle, so it accumulates in plasma. The liver, seeing no insulin signal, interprets the situation as starvation and pours out still more glucose. Adipose tissue releases free fatty acids, which the liver converts to ketone bodies — acetoacetate, beta-hydroxybutyrate and acetone — as an alternative fuel. That is the whole of diabetic ketoacidosis in one sentence: the cells are starving in a sea of sugar, and the liver keeps setting the table.

Once plasma glucose exceeds the renal threshold of roughly 180 mg/dL, the proximal tubule cannot reabsorb it all and glucose spills into urine. Glucose is osmotically active, so it drags water and electrolytes with it. This osmotic diuresis is why the classic presentation is polyuria and polydipsia, why the patient is volume depleted before anyone thinks to check a set of orthostatics, and why sodium, potassium, magnesium and phosphate all leave the body through the bladder while the serum values may still look deceptively normal.

Type 1: the beta cells are gone

Type 1 diabetes is autoimmune destruction of beta cells — a T-cell mediated insulitis that unfolds over months to years in a genetically susceptible person, often after a viral trigger. By the time hyperglycaemia appears, roughly 80 to 90 percent of beta-cell mass is already lost. Autoantibodies to glutamic acid decarboxylase 65 (GAD65), islet antigen 2, insulin and zinc transporter 8 are typically detectable, and C-peptide — the fragment cleaved from proinsulin when the body makes its own insulin — is low or undetectable. That C-peptide value is how a laboratory distinguishes a patient making no insulin from one making plenty but using it badly.

Presentation is fast and dramatic: days to a few weeks of polyuria, polydipsia, polyphagia and weight loss, often in a child, adolescent or young adult, and roughly a third of new cases arrive already in ketoacidosis. Because there is no endogenous insulin at all, these patients are ketosis prone and require exogenous insulin from diagnosis, permanently. There is no such thing as skipping the basal dose. A brief “honeymoon phase” of partial remission after starting insulin can fool families into thinking the disease resolved — it has not, and teaching should say so plainly.

Do not assume type 1 means young. Latent autoimmune diabetes in adults (LADA) is a slower autoimmune process presenting in the thirties, forties or later, frequently misclassified as type 2 until oral agents fail unusually quickly. A lean adult whose glucose control deteriorates within a year or two of diagnosis, or who arrives with ketones, deserves antibody and C-peptide testing.

Type 2: the insulin is there and nobody is listening

Type 2 diabetes begins with insulin resistance in muscle, liver and fat, usually driven by visceral adiposity, inactivity and genetics. The pancreas compensates by making more insulin, and for years it succeeds — the patient is hyperinsulinaemic and euglycaemic and has no idea. Over time the beta cells cannot sustain the output, secretion declines, and glucose rises first after meals, then fasting. Because there is still some circulating insulin, lipolysis stays largely suppressed and ketones usually do not accumulate. That single fact is why type 2 patients decompensate into a hyperosmolar, non-ketotic state rather than into ketoacidosis.

Onset is insidious, and the diagnosis is frequently made by a complication rather than a symptom. A patient presents with a non-healing foot ulcer, recurrent vaginal candidiasis, blurred vision, an unexpected myocardial infarction or a routine A1C drawn before surgery. Look for acanthosis nigricans — velvety hyperpigmentation in the axillae and posterior neck — and for the rest of the metabolic syndrome: central obesity, hypertension, elevated triglycerides, low HDL.

Two other categories matter on a medical-surgical floor. Secondary diabetes follows pancreatitis, pancreatectomy, Cushing syndrome, acromegaly, or drugs — glucocorticoids above all, plus thiazides, atypical antipsychotics, tacrolimus and some antiretrovirals. Steroid-induced hyperglycaemia is a daily reality: prednisone given each morning produces a predictable afternoon and evening glucose surge with a relatively normal fasting value, so the insulin adjustment belongs in the middle of the day, not at bedtime. Gestational diabetes is hyperglycaemia first recognised in pregnancy; it usually resolves at delivery but confers a lifetime type 2 risk that warrants screening every one to three years afterwards.

Making the diagnosis

Four tests establish diabetes, and any one of them will do — but in an asymptomatic patient the abnormal result must be confirmed, either by repeating the same test on a new sample or by a second different test from the same sample. A patient with unequivocal hyperglycaemic symptoms and a random glucose of 200 mg/dL or more needs no confirmation. Note that the A1C reflects average glycaemia over roughly the preceding three months, the lifespan of a red cell, and is therefore unreliable in haemoglobinopathies, recent transfusion, haemolysis, iron-deficiency anaemia, pregnancy and advanced chronic kidney disease.

Screen asymptomatic adults beginning at age 35, and earlier at any age with a BMI of 25 kg/m² or more (23 in Asian Americans) plus one risk factor — first-degree relative with diabetes, high-risk race or ethnicity, history of cardiovascular disease, hypertension, HDL below 35 mg/dL or triglycerides above 250 mg/dL, polycystic ovary syndrome, physical inactivity, acanthosis nigricans, or prior gestational diabetes. Repeat at least every three years if normal, annually in prediabetes. Prediabetes is not a benign label: intensive lifestyle intervention aiming at seven percent weight loss and 150 minutes of weekly activity reduces progression more effectively than metformin does, and it is the single highest-yield teaching conversation in primary care.

Section 2Assessment, Diagnostics and Surveillance

The history and physical that actually changes management

Start with the glycaemic history, not the diagnosis list. What is the regimen, in units and in times of day — and what does the patient actually take at home, which is frequently a different answer? When was the last dose? Has anyone been checking glucose, how often, and what have the numbers looked like? Any hypoglycaemic episodes, and did the patient feel them coming? Any hospitalisations for high or low sugars? Who fills the prescriptions, and can they afford them? Insulin rationing is a real and lethal cause of ketoacidosis, and patients rarely volunteer it unless asked without judgement.

Symptoms of hyperglycaemia are the three P’s plus fatigue: polyuria, polydipsia, polyphagia, blurred vision from osmotic lens swelling, weight loss, slow wound healing, recurrent yeast or urinary infections. Symptoms of hypoglycaemia divide into two groups you should keep separate in your head because they appear at different thresholds. Autonomic or adrenergic symptoms come first, usually below 70 mg/dL — tremor, palpitations, anxiety, diaphoresis, hunger, pallor. Neuroglycopenic symptoms come as the brain runs out of substrate, usually below 54 mg/dL — confusion, slurred speech, blurred or double vision, incoordination, bizarre behaviour, seizure, coma.

The physical examination is largely a search for complications. Take a supine and standing blood pressure. Inspect the mouth for candidiasis and periodontal disease. Auscultate for carotid bruits. Palpate dorsalis pedis and posterior tibial pulses and note capillary refill and hair distribution on the lower legs. Take both shoes and both socks off — every time, on every diabetic patient, no exceptions — and inspect the plantar surfaces, the heels and between every toe. Examine injection sites for lipohypertrophy, the rubbery subcutaneous thickening that develops where a patient injects repeatedly into the same spot, and which makes insulin absorption erratic and unpredictable.

Glycaemic monitoring: A1C, fingersticks and continuous sensors

The A1C measures the fraction of haemoglobin that has been non-enzymatically glycated, and it correlates to an estimated average glucose: an A1C of 6% corresponds to roughly 126 mg/dL, 7% to about 154, 8% to about 183, 9% to about 212, and 10% to about 240. Check it every three months when therapy has changed or the target is not met, and every six months when the patient is stable at goal. The general adult target is below 7%, but a target is a clinical judgement, not a reflex — below 6.5% for a young patient with long life expectancy and no hypoglycaemia risk, and a looser ceiling of below 8% for a frail elder with limited life expectancy, cognitive impairment, advanced complications or hypoglycaemia unawareness, where the harm of a low sugar plainly outweighs the benefit of a tight one. Read that looser figure as an upper limit to stay under, never as a number to climb to; and in very poor health or at end of life, stop managing to an A1C at all and manage instead to glucose values, avoiding both hypoglycaemia and symptomatic hyperglycaemia.

Capillary glucose targets for most non-pregnant adults are 80 to 130 mg/dL before meals and below 180 mg/dL at the peak, one to two hours after the start of a meal. Continuous glucose monitoring adds a metric worth knowing by name: time in range, the percentage of readings between 70 and 180 mg/dL, with a goal above 70 percent, less than 4 percent of time below 70 mg/dL and less than 1 percent below 54 mg/dL. Sensors report interstitial glucose, which lags plasma by five to fifteen minutes, so when a sensor value and the patient’s symptoms disagree — or when the glucose is falling rapidly — confirm with a fingerstick before you act.

Two patterns of morning hyperglycaemia are commonly confused and are distinguished by a single 0200–0300 glucose check. The dawn phenomenon is a physiological pre-waking surge of growth hormone and cortisol; the 3 a.m. glucose is normal or high and rises further by morning, and the fix is more or later-timed basal insulin. The Somogyi effect is rebound hyperglycaemia after unrecognised nocturnal hypoglycaemia; the 3 a.m. glucose is low, and the fix is less evening insulin or a bedtime snack. Adding insulin to a Somogyi pattern makes the patient worse, which is exactly why the 3 a.m. check is worth the interrupted sleep.

Complication surveillance is a schedule, not an impulse

The chronic complications of diabetes are silent until they are not, so the surveillance calendar is itself a nursing intervention. Ask about it at every encounter and document the gaps — discharge teaching that includes “you are due for your eye exam” is worth more than another lecture on carbohydrates.

The 10-gram Semmes-Weinstein monofilament test deserves a specific description because students are often asked to perform it. With the patient’s eyes closed, touch the filament perpendicular to the plantar skin at standard sites until it buckles into a C shape, hold about one second, and ask the patient to say when and where it is felt. Avoid callus, ulcer and scar. Inability to feel the buckling filament at any tested site means loss of protective sensation — that patient can stand on a tack, or wear a shoe with a pebble in it all day, and never know. Everything about their footwear teaching changes from that moment.

Section 3Insulin and the Non-Insulin Agents

Insulin by onset, peak and duration

Every insulin question you will ever be asked reduces to a timeline. If you know when the drug peaks, you know when the patient is most likely to go low, when the tray must be in front of them, and when to schedule the fingerstick. Memorise the table below as a shape, not as trivia.

Mixing rules are narrow and absolute. Only NPH and regular are mixed in the same syringe: inject air into the NPH (cloudy) vial, inject air into the regular (clear) vial, then draw up the regular first — clear before cloudy, so that no cloudy NPH contaminates the clear vial. Administer within five minutes of mixing. Glargine, detemir and degludec are never mixed with anything and never diluted. Premixed products such as 70/30 NPH-regular or 75/25 lispro protamine-lispro carry the peak profile of their intermediate component and demand a fixed, reliable meal schedule.

Insulin is a high-alert drug and should be handled like one

Insulin appears near the top of every list of medications most frequently involved in fatal error. Use an insulin syringe only — never a tuberculin or standard syringe — and match the syringe to the concentration. Never write or accept the abbreviation “U” for units; “10U” has been read as 100. Perform an independent double check of the drug, concentration, dose and pump settings with a second nurse per facility policy, particularly for any insulin infusion, any paediatric dose and any concentrated product (U-200 lispro, U-300 glargine, U-500 regular).

Insulin pens are single-patient devices, period. Even with the needle changed, biological material can be aspirated back into the cartridge, and pens have transmitted bloodborne infection between patients. Label the pen with the patient name and keep it in that patient’s drawer. Prime with two units before each injection to clear air, inject at a 90-degree angle, and count to ten before withdrawing the needle so the full dose is delivered rather than tracking back out.

Absorption varies by site — abdomen is fastest, then upper arm, then thigh, then buttock — so teach the patient to use one anatomic region consistently for a given injection and to rotate systematically within it, about an inch apart, avoiding a two-inch radius around the umbilicus. Exercise of a limb, heat, massage and hot showers all accelerate absorption from that site. Unopened vials and pens are refrigerated until the printed expiry; once in use, most products are kept at room temperature and discarded after 28 days (some, including detemir and degludec, allow longer — check the package). Never freeze insulin, never use it if it is discoloured, clumped or frosted-looking, and do not inject cold insulin, which stings.

Non-insulin agents, grouped by what they do

Whether a drug causes hypoglycaemia on its own is entirely a function of mechanism. Agents that force insulin release regardless of glucose — sulfonylureas and meglitinides — do. Agents that improve sensitivity, slow absorption, promote glucose loss in urine or act only in the presence of a rising glucose generally do not, unless combined with insulin or a secretagogue.

Glycaemic management in the hospitalised patient

Inpatient targets are deliberately looser than outpatient ones because the hospitalised patient eats unpredictably, receives steroids, goes NPO for procedures and has less physiological reserve for a low. Aim for 140 to 180 mg/dL for most critically ill and non-critically ill inpatients; a tighter 110 to 140 band is reasonable only for selected patients when it can be achieved without hypoglycaemia. Below 100 mg/dL, reassess the regimen; below 70, treat and change something.

A basal-bolus-correction regimen — long-acting insulin for background needs, rapid-acting insulin with meals, and a correction scale for the gap — is superior to sliding-scale insulin used alone. Sliding scale alone is reactive: it treats a high number after it has already happened, produces rollercoaster control, and is specifically inappropriate as sole therapy in type 1 diabetes. Time your fingersticks to the regimen: before meals and at bedtime for the eating patient, every four to six hours for the NPO patient, and hourly for anyone on an insulin infusion.

Watch the situations that predictably destabilise glucose: enteral feeding started or interrupted (an abrupt tube-feed hold with prandial coverage already given is a classic hypoglycaemic event), parenteral nutrition, glucocorticoids, octreotide, vasopressors, dialysis and any acute illness. And know that hypoglycaemia in a hospitalised patient is a reportable safety event in most facilities, not a private nursing footnote.

Section 4The Acute Crises: Hypoglycaemia, DKA and HHS

Hypoglycaemia is the emergency that kills first

Between a glucose of 40 and a glucose of 400, treat the 40. Hyperglycaemia damages the patient over hours to years; hypoglycaemia damages the brain in minutes. Level 1 hypoglycaemia is a glucose below 70 mg/dL, level 2 is below 54 mg/dL (clinically significant neuroglycopenia), and level 3 is severe hypoglycaemia of any value causing cognitive impairment requiring another person’s assistance.

For the conscious patient who can swallow safely, use the rule of 15: give 15 grams of fast-acting carbohydrate, wait 15 minutes, recheck. Fifteen grams is four glucose tablets, 4 ounces (half a cup) of juice or regular soda, one tablespoon of honey or sugar, or 8 ounces of milk. Repeat the cycle until the glucose is above 70 mg/dL, then give a snack containing protein and complex carbohydrate if the next meal is more than an hour away. Avoid chocolate, ice cream and peanut butter as the initial treatment — fat slows gastric emptying and delays the rise. Never put food or fluid in the mouth of a patient who is not fully awake and able to protect the airway.

For the unresponsive patient, the patient having a seizure, or anyone NPO or unable to swallow: if IV access exists, give 25 to 50 mL of 50% dextrose (12.5 to 25 g) by slow IV push per protocol, then start or resume a dextrose-containing infusion, because a D50 push wears off quickly. If there is no IV access, give glucagon 1 mg intramuscularly or subcutaneously, or 3 mg intranasally, and turn the patient onto their side — glucagon frequently causes vomiting. Glucagon mobilises hepatic glycogen, so it works poorly in the malnourished, the alcohol-intoxicated and anyone with depleted stores; those patients need dextrose. Recheck in 15 minutes, feed as soon as the patient is alert and safe, then investigate the cause. A sulfonylurea-induced or long-acting-insulin-induced low will relapse: that patient stays, gets a dextrose infusion and serial checks, and does not go home from the emergency department.

Hypoglycaemia unawareness is the loss of adrenergic warning symptoms, seen with autonomic neuropathy, long-duration diabetes, repeated lows and beta-blocker therapy. Beta blockers blunt tremor and tachycardia but not diaphoresis — so in a beta-blocked patient, sudden unexplained sweating is your warning sign. Treatment for unawareness is deliberately relaxing targets and scrupulously avoiding lows for several weeks, which restores symptom perception.

DKA and HHS side by side

Both are hyperglycaemic emergencies, both are usually precipitated by infection, non-adherence or a new stressor such as myocardial infarction, stroke, pancreatitis, trauma, surgery or a new drug. The difference is whether enough insulin remains to suppress lipolysis.

Two calculations belong in your pocket. Anion gap equals sodium minus the sum of chloride and bicarbonate; it is the metric of ketoacid accumulation and its closure — not the glucose — tells you the DKA is resolving. Effective serum osmolality equals two times the sodium plus glucose divided by 18; above 320 mOsm/kg it correlates with the obtundation of HHS, and a patient who is not fully alert with an osmolality below 320 needs a hunt for another cause of altered mentation. Remember also that hyperglycaemia dilutes serum sodium: add roughly 1.6 mEq/L to the measured sodium for every 100 mg/dL of glucose above 100 to get the corrected value that guides fluid choice.

The treatment sequence — fluids, potassium, insulin, and dextrose

Fluids first. Start isotonic 0.9% sodium chloride at roughly 15 to 20 mL/kg in the first hour (commonly 1 to 1.5 L in an adult), guided by haemodynamics and cardiac and renal status. After the initial resuscitation, the fluid is chosen by the corrected sodium: if it is normal or high, switch to 0.45% sodium chloride at 250 to 500 mL/h; if it is low, continue 0.9%. Volume alone lowers glucose substantially by dilution and restored renal perfusion, and it is the intervention that reverses the shock physiology. Monitor intake and output hourly, and in the elderly or anyone with heart failure or chronic kidney disease, watch for the crackles and jugular distension of overshoot.

Potassium before insulin. This is the sentence to carry out of this chapter. Total body potassium is severely depleted in both crises — on the order of 3 to 5 mEq/kg — even though the serum value on arrival is often normal or high, because acidosis and insulin deficiency have shifted potassium out of cells. Insulin drives potassium straight back in, and if you start the drip on a hypokalaemic patient you can precipitate lethal arrhythmia and respiratory muscle weakness. The rule: if serum potassium is below 3.3 mEq/L, hold the insulin and replace potassium (about 20 to 30 mEq/h) until it exceeds 3.3. If potassium is 3.3 to 5.2, run insulin and add 20 to 30 mEq of potassium to each litre of fluid to keep it in the 4 to 5 range. If it is above 5.2, withhold potassium, start insulin, and recheck in two hours. Confirm urine output before giving potassium, and keep the patient on continuous cardiac monitoring throughout.

Then insulin. Regular insulin is the only insulin given intravenously: a continuous infusion at 0.1 unit/kg/h, with or without an initial 0.1 unit/kg bolus (0.14 unit/kg/h if no bolus is used). Prime the tubing with the insulin solution before connecting it, because insulin adsorbs to plastic and the first millilitres are effectively wasted. Aim for a glucose fall of 50 to 75 mg/dL per hour; a faster drop risks cerebral oedema, particularly in children and adolescents, and a plateau usually means the fluid or insulin rate is inadequate. In HHS, insulin doses are lower and fluid resuscitation is proportionally more important.

Then dextrose. When the glucose reaches about 200 mg/dL in DKA, or about 250 to 300 mg/dL in HHS, change the fluid to one containing 5% dextrose and reduce the insulin infusion to roughly 0.02 to 0.05 unit/kg/h. This looks paradoxical to students — giving sugar to a hyperglycaemic patient — but the insulin must keep running to close the anion gap and stop ketogenesis, and dextrose is what makes that safe. DKA is resolved when the glucose is below 200 mg/dL plus two of: bicarbonate 15 mEq/L or higher, venous pH above 7.30, anion gap 12 mEq/L or less. Bicarbonate therapy is reserved for a pH below 6.9. Phosphate is replaced only for a level below 1.0 mg/dL with cardiac dysfunction, respiratory depression or haemolytic anaemia.

What you monitor and what makes you call

During active treatment expect hourly capillary glucose, basic metabolic panel every two to four hours, continuous cardiac monitoring, strict hourly intake and output, and neurologic checks. Falling mental status during treatment — especially in a young patient whose numbers are improving — is cerebral oedema until proven otherwise: headache, vomiting, bradycardia with rising blood pressure, then deterioration. Stop and escalate immediately.

Do not forget euglycaemic ketoacidosis. Patients taking an SGLT2 inhibitor, pregnant patients, and those who have been vomiting or eating nothing can be fully ketoacidotic with a glucose under 250 mg/dL. If the patient is nauseated, tachypnoeic and acidotic, check ketones and a gas regardless of how reassuring the glucose looks. And in every case, find the precipitant: culture, chest film, ECG, medication review. Treating the DKA without treating the pyelonephritis that caused it simply buys you a second admission.

Here is the escalation you should be able to give without notes. S: “This is Priya, RN, on 5-West with Mr. Alvarez in 512, a 24-year-old with type 1 diabetes admitted with vomiting.” B: “He was admitted this morning; he ran out of insulin four days ago.” A: “In the last hour his respirations have gone from 18 to 32 and deep, he is drowsy, his glucose is 486, his breath smells fruity and his blood pressure has dropped from 118/70 to 92/54 with a heart rate of 128.” R: “I think he is in DKA. I need you to see him now. I would like a stat basic metabolic panel, serum beta-hydroxybutyrate, venous blood gas, magnesium and phosphorus, a large-bore IV with isotonic fluid, and orders for an insulin infusion and cardiac monitoring.”

Section 5Chronic Complications, Teaching and Discharge

Microvascular disease: eyes, kidneys, nerves

Chronic hyperglycaemia glycates proteins and thickens basement membranes throughout the microcirculation. In the retina this produces diabetic retinopathy — non-proliferative changes of microaneurysms, dot-and-blot haemorrhages and hard exudates, progressing to proliferative retinopathy with fragile neovascular vessels that bleed into the vitreous or drag the retina off. It is asymptomatic until it is severe, which is the entire argument for the annual dilated examination. Sudden painless vision loss, a shower of new floaters or a “curtain” across the field is a same-day ophthalmology emergency. Diabetic macular oedema is the more common cause of gradual central vision loss and is treated with intravitreal anti-VEGF injections.

Diabetic kidney disease begins with hyperfiltration, then persistent albuminuria at a urine albumin-to-creatinine ratio of 30 mg/g or higher, then declining eGFR. An ACE inhibitor or ARB is indicated for albuminuria with hypertension and slows progression by reducing intraglomerular pressure; monitor potassium and creatinine after starting or increasing the dose, and expect a modest creatinine rise that is acceptable. SGLT2 inhibitors and, increasingly, non-steroidal mineralocorticoid antagonists add further renal protection. Blood pressure control below 130/80 mmHg matters at least as much as glucose control here. As eGFR falls, insulin clearance falls with it and insulin requirements paradoxically decrease — a patient with worsening kidney function who suddenly starts running low is telling you something about their kidneys, not their diet.

Diabetic neuropathy is most often a distal symmetric polyneuropathy in a stocking-glove distribution: numbness, tingling, burning and lancinating pain that is worse at night, with loss of vibratory sense and ankle reflexes early. Pharmacological options include pregabalin, gabapentin, duloxetine and amitriptyline; opioids are not first-line. Autonomic neuropathy is the quieter and more dangerous form — orthostatic hypotension, resting tachycardia, silent myocardial ischaemia, gastroparesis, neurogenic bladder with retention and overflow, erectile dysfunction, and hypoglycaemia unawareness. Gastroparesis produces early satiety, bloating and wildly erratic post-meal glucose; manage with small, frequent, low-fat, low-fibre meals, and note that metoclopramide carries a boxed warning for tardive dyskinesia and is limited to under 12 weeks.

Macrovascular disease and the diabetic foot

Atherosclerotic cardiovascular disease is the leading cause of death in diabetes, and diabetes is a coronary risk equivalent. Because of autonomic neuropathy, myocardial infarction may present without chest pain — as dyspnoea, fatigue, nausea, confusion or simply unexplained hyperglycaemia. Take “I just feel off” in a diabetic patient as seriously as crushing substernal pain in anyone else and obtain an ECG. Peripheral arterial disease produces claudication, diminished pulses, hair loss, dependent rubor and cool, shiny, thin skin; cerebrovascular disease produces stroke, which Chapter 3 takes up in detail.

The diabetic foot ulcer is where neuropathy, ischaemia and immune dysfunction meet, and it precedes the majority of non-traumatic lower-limb amputations. Neuropathy removes the pain that would otherwise stop the patient from walking on a wound; motor neuropathy deforms the arch and toes so pressure concentrates under the metatarsal heads; ischaemia starves the healing; hyperglycaemia impairs neutrophil function. Assessment of any ulcer records site, size in centimetres, depth, undermining, wound bed appearance, exudate, odour, surrounding callus or cellulitis, and whether bone is palpable on gentle probing — a positive probe-to-bone strongly suggests osteomyelitis. Management combines pressure offloading, debridement, moist wound care, targeted antibiotics for infection and vascular assessment. Note that a warm, red, swollen, relatively painless foot in a neuropathic patient may be Charcot neuroarthropathy rather than infection, and it requires immediate immobilisation to prevent midfoot collapse.

Foot teaching is concrete and non-negotiable. Inspect both feet daily, using a mirror or a family member for the soles. Wash daily in lukewarm water tested with a thermometer or the elbow — never the foot — and dry carefully between the toes. Moisturise the tops and bottoms but not between the toes. Cut nails straight across, or have podiatry do it. Never use over-the-counter corn removers, razor blades or heating pads. Never go barefoot, indoors or out. Shake out every shoe before putting it on. Break in new shoes 1 to 2 hours a day. Wear seamless, non-constricting socks. Report any blister, cut, redness, callus, ingrown nail or colour change the day it appears — not at the next scheduled visit.

Self-management teaching and sick-day rules

Discharge teaching is prioritised by what will kill the patient soonest if missed: hypoglycaemia recognition and treatment first, insulin administration technique second, sick-day rules third, then foot care, monitoring, nutrition and follow-up. Use teach-back for every psychomotor skill. Watch the patient draw up and inject their own dose before they leave, and watch the caregiver do it too. Ask directly about cost, refrigeration, vision, dexterity, literacy and transport, because the most elegant regimen fails against a broken refrigerator or a $300 copay.

Nutrition teaching centres on consistent carbohydrate intake, portion awareness (the plate method: half non-starchy vegetables, one quarter lean protein, one quarter starch) and carbohydrate counting for those on prandial insulin, where a typical starting ratio is one unit per 15 grams. Emphasise fibre, whole grains and limited added sugar and saturated fat. Alcohol inhibits hepatic gluconeogenesis and can cause delayed hypoglycaemia many hours later — teach patients to drink only with food, in moderation, and to check glucose before bed. Physical activity of 150 minutes per week improves insulin sensitivity for up to 48 hours; teach patients on insulin or secretagogues to check before, sometimes during and after exercise, to carry fast carbohydrate, and to avoid injecting into a limb about to be exercised. Do not exercise if the glucose is above 250 mg/dL with ketones present — exercise will worsen ketosis.

Sick-day rules prevent most avoidable hyperglycaemic crises, and they are counterintuitive enough that they must be taught explicitly and rehearsed. Illness raises counter-regulatory hormones, so glucose and insulin needs go up even when the patient is eating less.

The older adult, delegation and the red flags

Older adults present differently and are more fragile in both directions. Hypoglycaemia in an elder rarely looks like tremor and diaphoresis — it looks like a fall, a new confusion, slurred speech mistaken for stroke, or a family member saying “she is just not herself.” Check a glucose on every older adult with altered mental status, every time. Hyperglycaemia likewise presents atypically as new incontinence, delirium, weakness or dehydration, and because the thirst mechanism blunts with age and mobility may prevent reaching a glass of water, HHS develops quietly over days. Renal clearance declines, so sulfonylureas and renally cleared insulins accumulate; glyburide is on the Beers list and should be avoided. Glycaemic targets loosen deliberately — an A1C below 7.5% for a healthy older adult and below 8.0% with multiple comorbidities or cognitive impairment — upper limits, not goals to drift up to — while in very poor health or at end of life there is no A1C target at all, only glucose values managed to avoid hypoglycaemia and symptomatic hyperglycaemia. Polypharmacy, vision loss, arthritic hands and cost all bear directly on whether a regimen can be executed at home.

Delegation follows one principle: the nursing process cannot be delegated. Assessment, teaching, evaluation, clinical judgement and any unstable patient remain with the RN. Assistive personnel may, within facility policy and training, obtain point-of-care capillary glucose readings, record intake and output, assist with meals and positioning, obtain vital signs on stable patients, and report observations such as a reddened heel or an untouched tray — and they must be told explicitly which values to report immediately and to whom. Insulin administration, insulin infusion titration, evaluating whether a hypoglycaemic episode has resolved, initial teaching of injection technique, and the assessment of a new foot ulcer are RN responsibilities. A licensed practical or vocational nurse may administer subcutaneous insulin and reinforce previously taught content within state scope and policy, but the initial assessment, the initial teaching and the unstable patient stay with the registered nurse.

Words worth knowing