Endocrinology

Matthew Sims

Outline

Station 6.1: Diabetic ketoacidosis

Station 6.2: Hyperosmolar hyperglycaemic state (HHS)

Station 6.3: Hypoglycaemia

Station 6.4: Insulin prescribing

Station 6.5: Hyperkalaemia

Station 6.6: Hypercalcaemia

Station 6.7: Hyponatraemia

Station 6.8: Addisonian crisis

Station 6.9: Hyperthyroid crisis (thyroid storm)

Station 6.10: Hypothyroidism

Station 6.1: Diabetic ketoacidosis

You are the junior doctor on the medical admission unit, and are seeing a 21-year-old girl, Ms Brown, who has come in with shortness of breath, abdominal pain and vomiting. She is too confused to give you much history, but her mother tells you she has recently been mildly unwell with painful micturition, and had been told by her GP that she had a urinary tract infection. She has been drinking a lot of water, and using the bathroom frequently over the past week. She has no past medical history.

Patient Details

Name:	Sarah Brown
DOB:	11/11/1993
Hospital Number:	204684560
Weight:	70 kg (estimated)
Height:	172 cm (estimated)
Consultant:	Dr Brown
Hospital/Ward:	WGH 2B
Current Medications:	Nil
Allergies:	Nil
Admission date:	02/02/2014

Triggers of DKA

New diagnosis

Insulin omission

Inadequate insulin dosing

Infection

Myocardial infarction

Complications of diabetes

Microvascular: retinopathy, neuropathy, nephropathy

Macrovascular: ischaemic heart disease, peripheral arterial disease, cerebrovascular accidents/TIAs

Infection

DKA management summary

Fluid resuscitation

Fixed rate insulin infusion

Identifying cause of DKA

Initial Assessment

Airway

Assess patency of the airway

‘Airway is patent, and there are no snoring or other noises. Her breath smells strongly of nail polish remover.’

No action is currently required.

Breathing

Assess respiratory rate, oxygen saturations and work of breathing. Look for Kussmaul breathing. Listen for evidence of lower respiratory tract infection

‘RR is 40/min. Sats are 99% on air, with good bilateral air entry and no additional breath sounds. The patient’s breaths are deep and sighing.’

No action is currently required.

Circulation

Assess pulse, blood pressure, CRT, and signs of dehydration. In DKA, shock may occur due to osmotic diuresis, diarrhoea, and/or precipitating infection

‘The patient is warm to touch. Her radial pulse feels bounding and regular, 128 bpm. CRT is 3 seconds. BP is 104/68 mmHg.

The patient is shocked: obtain large bore IV access, send off bloods, and prescribe a fluid bolus. Ask the nursing staff to put the patient on continuous ECG monitoring and pulse oximetry. Catheterization may be required to allow accurate fluid balance.

Prescribe (see Figs 6.1–6.3)

Fluid challenge, e.g. 500 mL 0.9% SODIUM CHLORIDE IV (over 15 mins)

Antipyretics, e.g. PARACETAMOL 1 g ORAL STAT

Antibiotics, e.g. CO-AMOXICLAV (1000 mg/200 mg) 1.2 g IV STAT, GENTAMICIN 350 mg IV (over 1 H) STAT (5 mg/kg, estimating patient weight as 70 kg). In this case it’s unlikely the gentamicin will need to be continued as a regular prescription unless an MCS result demonstrates resistance to penicillins.

Figure 6.1

Figure 6.2

Figure 6.3

Disability

Assess GCS and blood sugar. Ketosis and/or current infection may make the patient obtunded

‘GCS is 14/15. Capillary blood glucose is 33.2 mmol/L.’

You suspect now that this is a case of diabetic ketoacidosis, and start insulin therapy (see initial management).

Exposure

Look for evidence of possible triggers for DKA, particularly infection. In this case, there is a specific concern about a UTI, so look for evidence of pyelonephritis. Measure temperature

‘There is marked renal angle tenderness on the right side. Temperature is 39.1°C.’

There is strong clinical evidence the patient has pyelonephritis. There is a need for broad-spectrum antibiotic cover. One possible option would be a penicillin plus an aminoglycoside. Paracetamol should be given as an antipyretic.

Initial Investigations

VBG: Assess for metabolic acidaemia (due to ketosis)

Capillary or urinary ketone measurement: Capillary is preferred if available. Capillary ketones are a measure of 3-hydroxybutyrate. Urinary ketones measurement includes 3-hydroxybutyrate and acetoacetone, but is less precise and subject to inter-reader variability

FBC, U&Es, chloride, bicarbonate, plasma glucose, CRP, and blood cultures: Looking for evidence of infection, renal failure, and to confirm the glucose level. In the context of a metabolic acidaemia, bicarbonate and chloride are useful to calculate the anion gap

Troponin: Indicated in patients with chest pain/high risk of ischaemic heart disease–not in this case

CXR: Part of a septic screen

Urine dipstick: Look for leucocytes and/or nitrites, which would be consistent with infection

Pregnancy test: If detected, current pregnancy would impact upon the investigation and management of this patient. Her abdominal pain could be related to a complication of pregnancy

Renal USS: To help confirm the diagnosis of pyelonephritis

DKA definition

Ketonaemia≥3 or ketonuria>2

Blood glucose>11 mmol/L or known diabetes mellitus

pH<7.3 and/or bicarbonate<15 mmol/L

‘VBG: pH 7.11, PCO₂3.8 kPa, HCO₃5.8 mmol/L, BE−21.2 mmol/L. Capillary ketones are 6 mmol/L. Hb 125 g/L, WCC 17×10⁹/L, neutrophil 15.6×10⁹/L, platelet 198×10⁹/L. CRP 250 mg/L. Urea 12.3 mmol/L, creatinine 134 µmol/L, Na 146 mmol/L, K 5.8 mmol/L, Cl 99 mmol/L. Glucose 31 mmol/L. Anion gap is 47 mmol/L [(Na+K)−(Cl+HCO₃)=(146+5.8)−(99+5.8)=47 mmol/L]. CXR is normal. Urine dipstick+1 nitrites,+1 leucocytes.’

Table 6.1

Sarah Brown’s blood results and VBG

Parameter	Value	Normal range (Units)
Haemoglobin	125 g/L	Men: 135–177 (g/L) Women: 115–155 (g/L)
WCC	17×10⁹/L	4–11 (×10⁹/L)
Neutrophil	15.6×10⁹/L	2.0–7.5 (×10⁹/L)
Lymphocyte	2×10⁹/L	1.5–4 (×10⁹/L)
Platelet	198×10⁹/L	150–400 (×10⁹/L)
CRP	250 mg/L	<5 (mg/L)
Urea	12.3 mmol/L	2.5–6.7 (mmol/L)
Creatinine	134 μmol/L	79–118 (μmol/L)
Sodium	146 mmol/L	135–146 (mmol/L)
Potassium	5.8 mmol/L	3.5–5.0 (mmol/L)
eGFR	>60 mL/min	>60 (mL/min)
Chloride	99 mmol/L	98–106 (mmol/L)
Plasma glucose	31 mmol/L	4.5–5.6 (mmol/L)
pH	7.11	7.35–7.45
PCO₂	3.8 kPa	4.8–6.1 (kPa)
Bicarbonate	5.8 mmol/L	22–26 (mmol/L)
BE	−21.2 mmol/L	±2 mmol/L

Blood gases

ABGs are more painful than taking VBGs. Unless there is a specific reason to look at PO₂, diagnosis and monitoring of the patient’s acid–base status can be done with VBGs.

Initial Management [1]

IV fluids: First priority is to rehydrate. Maintain good fluid balance by measuring hourly urine volumes and consider a catheter; 0.9% sodium chloride is the rehydration fluid of choice, to replace not only water, but also correct sodium and chloride deficits

In DKA, typical water deficit is 100 mL/kg, therefore for a 70 kg person, about 7 L of IV fluid may be needed in the first 24 hours. This should be given faster initially (i.e. 2–3×1 L bags over 1–2 hours), with regular titration of the rate depending on patient response (RR, HR, BP, urine output)

Fixed rate IV insulin infusion: This is not the same as a variable sliding scale (in which the rate of an insulin infusion is titrated against the blood glucose). The role of soluble insulin in DKA is to bring down the serum glucose but, more importantly, to suppress ketone production. Insulin should not be stopped until acidaemia has resolved and there is no remaining evidence of ketones

Insulin (Actrapid® or similar) should be commenced at 0.1 units/kg/h (70 kg×0.1 is 7 units/h in this case).

Continue or commence long-acting insulin analogues. This is to avoid rebound hyperglycaemia after discontinuation of IV insulin infusion. A typical starting dose for a normal weight person is 6 units of insulin glargine (Lantus®), although this can be altered depending on size (discuss with diabetes team)

Potassium replacement: Plasma potassium is often high on admission, but falls rapidly as IV insulin and fluid replacement are commenced. For this reason, it is important to monitor potassium regularly, and add potassium to ongoing maintenance fluids after initial resuscitation

Thromboprophylaxis: Sick medical patients are at risk of venous thromboembolism

Continue treatment of trigger: Regular co-amoxiclav should be given to treat the pyelonephritis (gentamicin here is given as a one off dose to broaden initial antibiotic cover). Give further paracetamol if temperature persists, or for any pain.

Prescribe (see Figs 6.1–6.3)

INSULIN (ACTRAPID®) 50 units in 50 mL of 0.9% SODIUM CHLORIDE (concentration 1 unit/mL) infusing at a rate of 7 mL/h (use fluid chart)

Antibiotics, e.g. CO-AMOXICLAV (1000 mg/200 mg) 1.2 g TDS IV

Thromboprophylaxis, e.g. DALTEPARIN 5000 units OD SC

Long-acting insulin, e.g. INSULIN GLARGINE (LANTUS®) 6 units OD at 18.00 h SC

Reassessment

You re-evaluate Ms Brown one hour after the insulin infusion is commenced. U&Es and venous blood gas are repeated

‘RR has fallen to 36/min, HR is now 118 bpm and BP is 112/67 mmHg. She still seems a little confused. VBG shows pH 7.13, PCO₂3.9 kPa, HCO₃7 mmol/L, BE−15 mmol/L. Glucose is 27 mmol/L. K is 5.5 mmol/L, and renal function is slightly improved.’

Table 6.2

Sarah Brown’s repeat blood results and VBG

Parameter	Value	Normal range (Units)
Urea	10 mmol/L	2.5–6.7 (mmol/L)
Creatinine	130 μmol/L	79–118 (μmol/L)
eGFR	>60 mL/min	>60 (mL/min)
Sodium	145 mmol/L	135–146 (mmol/L)
Potassium	5.5 mmol/L	3.5–5.0 (mmol/L)
Chloride	99 mmol/L	98–106 (mmol/L)
Plasma glucose	27 mmol/L	4.5–5.6 (mmol/L)
pH	7.13	7.35–7.45
PCO₂	3.9 kPa	4.8–6.1 (kPa)
HCO₃	7 mmol/L	22–26 (mmol/L)
BE	–15 mmol/L	±2 (mmol/L)

The patient’s HR and BP have responded to IV fluid, but she is still very fluid deplete.

Prescribe (see Figs 6.1–6.3)

Further fluids, e.g. 0.9% SODIUM CHLORIDE 1000 mL/h

Cerebral oedema

Although the mechanism has not clearly been elucidated, cerebral oedema can complicate DKA, and lead to death. It is more common in children and adolescents, therefore, in this group, cautious fluid replacement is made over 48 hours. In adults, guidelines suggest cautious fluid replacement in non-shocked, small, young adults [1].

Definitive Management [1]

Ongoing management of this patient should involve the inpatient specialist diabetes team, senior medical doctors, and HDU or ITU staff depending on the clinical condition. The aim should be to resolve the ketonaemia and acidosis within 24 hours.

Ongoing IV fluids: If the patient has clinically responded to initial fast fluids (i.e. good urine output, falling HR, increasing BP), then the remaining fluid deficit can be replaced more slowly, e.g. 0.9% sodium chloride every 4 hours, based on regular clinical assessment, including a review of fluid balance, checking for clinical evidence of overload (i.e. increasing RR, wet crepitations in chest, and peripheral oedema), and GCS

Ketone monitoring and insulin infusion: Blood ketones should be measured hourly. The target is a fall of≥0.5 mmol/L/h. If measurement of blood ketones is not available, then rate of glucose fall and bicarbonate increase can be used as proxies (see below). If the ketone target is not met, then increase the insulin infusion at 1 unit/h until this is achieved. The insulin infusion can be stopped when the ketones are less than 0.3 mmol/L and the venous pH>7.3

Glucose monitoring and 10% glucose solution: Blood glucose should be measured hourly. A reduction of 3 mmol/L/h or greater is the target. If the glucose falls below 14 mmol/L while the insulin infusion is still required, start 10% glucose at 125 mL/h. This is in addition to, not a replacement for, the 0.9% sodium chloride infusion, as the latter is more effective for replacement of circulatory volume

VBG monitoring: This is for the measurement of pH, bicarbonate and K⁺. Repeat at one hour after initial assessment then every 2 hours for the first 6 hours. Frequency of measurement thereafter depends on the progress of the patient. The target increase in bicarbonate is>3 mmol/L/h

With the introduction of insulin and IV rehydration, the potassium will start to fall. If K⁺ is between 3.5 and 5.5 mmol/L, replace 40 mmol of potassium chloride with every 1 L of fluid given (but do not give more than 10 mmol/h of potassium). If<3.5 mmol/L, then more concentrated potassium solutions are likely to be needed: this may well require HDU

Follow-on care: Once ketonaemia and acidosis have resolved, the patient should be encouraged to eat and drink. A subcutaneous insulin regimen, often basal—bolus, will be needed for newly diagnosed patients. Known diabetic patients should be restarted on their SC insulin regimen, although this may need to be adjusted. The inpatient diabetes team should be involved, including patient (re-)education.

Handing over the Patient

‘Ms Brown is a 21-year-old patient presenting with diabetic ketoacidosis, and sepsis secondary to pyelonephritis. This is a new diagnosis of Type 1 diabetes.

I’ve started her on IV 0.9% sodium chloride, she’s now on her 2nd litre over 1 hour. The insulin infusion has been commenced at a rate of 7 units/hour. She’s had co-amoxiclav and gentamicin to cover for urinary sepsis. Initial blood tests show a WCC of 17×10⁹/L and a CRP of 250 mg/L. Most recent K is 5.5 mmol/L, and venous gases are improving, with most recent one showing pH 7.13, PCO₂ 3.9 kPa, HCO₃ 7 mmol/L. Glucose is 27 mmol/L. Capillary ketones are 5.6 mmol/L, which is getting better. Urine and blood cultures have been sent.

Please repeat a VBG, capillary ketones, U&Es, and evaluate hydration status in one hour and prescribe further 0.9% sodium chloride±potassium chloride and, if needed, adjust the insulin infusion. She’s still in MAU at the moment. Given the level of nursing support she will require for at least the next 12 hours, I think we should ask medical HDU whether they will take her with a plan to step down to the ward the next day.’

Station 6.2: Hyperosmolar hyperglycaemic state (HHS)

You’re the junior doctor on nights in the Medical Assessment Unit. You are called to attend a 69-year-old woman, Mrs Jones. The nurses tell you she’s a frequent attender and is known to have Type 2 diabetes. She appears drowsy and is unaccompanied.

Patient Details

Name:	Helen Jones
DOB:	14/09/45
Hospital Number:	3299206023
Weight:	93 kg
Height:	151 cm
Consultant:	Dr Norris
Hospital/Ward:	WGH MAU
Current Medications:	Nil
Allergies:	Nil
Admission date:	02/02/14

Differential diagnosis of presenting complaint

Infection: chest, urine, gastroenteritis

Cardiovascular: MI, stroke

New presentation of Type 2 diabetes

Non-concordance with oral diabetic medications or insulin

Complications of HHS

Coma

Pressure sores

Cerebral oedema

Central pontine myelinolysis

Arterial or venous thromboses

Death

HHS Management summary

Fluid resuscitation

Potassium replacement

Insulin therapy (when indicated)

Identification of precipitant

Thromboprophylaxis

Initial Assessment

Airway

Assess patency of the airway

‘Airway is patent, and there are no snoring or other noises.’

No action is currently required.

Breathing

What is the respiratory rate, oxygen saturations, and work of breathing? Look for Kussmaul breathing. Listen for evidence of lower respiratory tract infection

‘Respiratory rate is 24/min, with sats of 85% on air, there are moist crackles audible at the right base.’

High-flow oxygen is needed with the aim of maintaining saturations of 94–98%.

Request a CXR.

Prescribe (see Figs 6.4–6.6)

HIGH-FLOW OXYGEN, e.g. 15 L/min via a NON-REBREATHER MASK

Fluid bolus, e.g. 0.9% SODIUM CHLORIDE 500 ml IV (over 15 min)

Figure 6.4

Figure 6.5

Figure 6.6

Circulation

Assess pulse, blood pressure, CRT, and look for signs of dehydration

‘CRT is 4 seconds. HR is 122 bpm, and blood pressure 103/71 mmHg. Her brow and hands feel warm to the touch.’

The patient is shocked: obtain large bore IV access, send off bloods, and prescribe a fluid challenge. Ask the nursing staff to put the patient on continuous ECG monitoring and pulse oximetry. Catheterization may be required to allow accurate fluid balance.

Disability

Assess GCS and blood sugar. Ketosis and/or current infection may make the patient obtunded

‘GCS is 14/15 as the patient is disorientated. The capillary blood glucose is 37.6 mmol/L, and there are no urinary or blood ketones.’

This suggests a diagnosis of HHS, and aggressive fluid resuscitation should be continued.

Exposure

Measure temperature and look for potential reasons that might explain the patient’s decompensation, particularly infection. Examine the skin carefully for evidence of cellulitis or infected ulcers, particularly on the heels. Also examine for abdominal tenderness or gastrointestinal upset, e.g. diarrhoea

‘Temperature is 38.1°C, there is no evidence of sores including pressure areas. The patient is obese, with a soft, non-tender abdomen.’

HHS: definition [2]

There are no strict criteria, but these are characteristic features:

Hypovolaemia

Hyperglycaemia (≥30 mmol/L) without significant ketonaemia (<3 mmol/L) or acidosis (pH>7.3, bicarbonate>15 mmol/L)

Osmolality≥320 mosmol/kg

Alterations to mental state are common in HHS secondary to raised osmolality. This is a spectrum from mild confusion through to coma.

Remember that HHS and DKA are not mutually exclusive and may coexist.

Given the patient is pyrexial with crepitations in her chest, she should be treated for pneumonia. Prescribe co-amoxiclav as a once off dose since renal function is not yet known. While the nurses are preparing this ensure blood cultures are taken

Prescribe antipyretics.

Prescribe (see Figs 6.4–6.6)

Antibiotics, e.g. CO-AMOXICLAV (1000 mg/200 mg) 1.2 g IV STAT

Antipyretics, e.g. PARACETAMOL 1 g ORAL STAT

Initial Investigations

VBG: For confirmatory blood glucose, rapid Na result, and to assess acid–base status. Acidaemia could occur secondary to ketosis, or sepsis (raised lactate)

Bloods: FBC, U&Es, LFTs, CRP, glucose, blood cultures. Electrolytes can be deranged due to HHS and with subsequent fluid infusions. If available, (lab measured) osmolality should be requested. If this is not available then calculate this using the formula 2×Na⁺+glucose+urea (estimated osmolality)

Capillary ketones: If available, otherwise look at urine ketones. This is important for determining whether insulin should be started earlier, and in determining whether this is DKA rather than HHS in situations where there is diagnostic doubt. If ketones are raised, they should be monitored

Urine dipstick: For markers of infection and for ketones

CXR: Look for consolidation

ECG: Look for evidence of cardiovascular precipitants of HHS including myocardial infarction

‘Bloods show Hb 134 g/L, WCC 16.7×10⁹/L, platelets 198×10⁹/L, urea 22 mmol/L, creatinine 170 μmol/L, K 3.7 mmol/L, Na 159 mmol/L. LFTs are normal. CRP is 123 mg/L. Glucose is 39 mmol/L. You calculate osmolality as 379 mosmol/kg (range 278–305). Capillary ketones are 0.3 mmol/L. Venous blood gas shows a metabolic acidosis with partial respiratory compensation. CXR shows consolidation at the right base. The ECG shows sinus tachycardia rate 116 bpm with no ST segment or T wave abnormalities.’

Table 6.3

Helen Jones’s blood results including VBG

Parameter	Value	Normal range (Units)
Haemoglobin	134 g/L	Men: 135–177 (g/L) Women: 115–155 (g/L)
WCC	16.7×10⁹/L	4–11 (×10⁹/L)
Neutrophil	15.6×10⁹/L	2.0–7.5 (×10⁹/L)
Lymphocyte	2×10⁹/L	1.4–4 (×10⁹/L)
Platelet	198×10⁹/L	150–400 (×10⁹/L)
CRP	123 mg/L	<5 (mg/L)
Urea	22 mmol/L	2.5–6.7 (mmol/L)
Creatinine	170 μmol/L	79–118 (μmol/L)
eGFR	40.4 mL/min	>60 (mL/min)
Sodium	159 mmol/L	135–145 (mmol/L)
Potassium	3.7 mmol/L	3.5–5.0 (mmol/L)
Plasma glucose	39 mmol/L	4.5–5.6 (mmol/L)
ALT	27 IU/L	<40 (IU/L)
ALP	92 IU/L	39–117 (IU/L)
Bilirubin	14 μmol/L	<17 (μmol/L)
pH	7.25	7.35–7.45
PaCO₂	3.8 kPa	4.8–6.1 (kPa)
Bicarbonate	12.1 mmol/L	22–26 (mmol/L)
BE	−13.5 mmol/L	±2 (mmol/L)

Initial Management [2]

IV fluids

IV fluids are used for the normalization of plasma osmolality, sodium, and glucose and to restore the circulating volume by replacing the considerable water and electrolyte deficit

In HHS, the plasma osmolality is significantly raised. High glucose is the significant contributor to this raised osmolality, but also plasma sodium and urea concentration are usually raised as well, further increasing the osmolality

There is a total body deficit of electrolytes (principally sodium, potassium, chloride), due to their renal loss secondary to an osmotic diuresis driven by glycosuria

The key to treating HHS is to avoid too rapid correction of osmolality, as this can be associated with seizures, cerebral oedema, and central pontine myelinolysis

Methods of avoiding rapid changes in osmolality include regular monitoring of clinical state, U&Es and plasma osmolality (see Definitive management). Furthermore, the rate of fluid administration needs to be carefully titrated and the fluid used should not be too hypotonic relative to the patient’s plasma. Therefore, 0.9% sodium chloride is the fluid of choice. In healthy patients, this is isotonic. In HHS patients, this is hypotonic. Therefore, 0.45% sodium chloride is too hypotonic and if used initially risks precipitating rapid osmotic shifts; 0.45% sodium chloride can be considered at a later stage in refractory cases when a more rapid osmotic shift is needed (see Definitive management)

In HHS, the extent of dehydration is typically more profound than in DKA, requiring up to 200 ml/kg of fluid replacement over 2 or more days.

Hourly urine volumes should be measured, therefore, consider a catheter particularly if the patient is immobile, confused, and/or incontinent.

Given Mrs Jones’s reduced GCS, she should be catheterized and started on a fluid balance chart

Insulin is not initially required: In the majority of cases, the plasma glucose should begin to correct with 0.9% sodium chloride alone. Remember there is no absolute insulin deficit. Indications for starting insulin immediately are blood ketones>1 or urine ketones>2, otherwise this should be initially postponed.

Replace potassium: This is required even if the potassium is within normal limits. Avoid giving potassium supplementation to those with K>5.5 mmol/L

Prescribe VTE prophylaxis: Patients with HHS are at high risk of VTE and should be prescribed LMWH. Mrs Jones’s Cockcroft–Gault creatinine clearance is 40.4 mL/min [(140–69)×93×1.04/170=40.4]. Anti-factor Xa level monitoring is only required in patients with an estimated GFR<20 mL/min, therefore, this may be required should her renal function worsen

Treat precipitant: In this case, this is likely to be a lower respiratory tract infection. She would qualify as severe community-acquired pneumonia (CURB 65 score=3 as over 65, confused, with a raised urea) and, therefore, add in clarithromycin 500 mg orally BD. Continue standard dose co-amoxiclav (it does not need to be renally adjusted until estimated GFR<30 mL/min). Paracetamol can be continued for pyrexia and pain control.

Prescribe (see Figs 6.4–6.6)

Further IV fluids, e.g. 0.9% SODIUM CHLORIDE 1 L with 20 mmol KCl 500 mL/h

Antibiotics, e.g. CLARITHROMYCIN 500 mg STAT ORAL, and then BD, CO-AMOXICLAV (1000 mg/200 mg) 1.2 g IV TDS

Thromboprophylaxis, e.g. DALTEPARIN 5000 units SC OD

Analgesia/antipyretic, e.g. PARACETAMOL 1 g ORAL QDS

Reassessment

You re-evaluate the patient 90 minutes after first presentation

‘Mrs Jones has a patent airway. Her sats are 100% on 15 L high-flow oxygen. Her RR is now down to 18 breaths per minute. Her HR is 110 bpm, and BP is 110/70 mmHg. Her temperature is now 37.0°C. She’s making orientated conversation with the nurses. She’s been catheterized and in the first half an hour she’s passed 45 mL of dark yellow urine. She’s on continuous ECG and sats monitoring and is still in MAU. Bloods taken 1 hour after presentation show urea 21 mmol/L, creatinine 165 μmol/L, K 3.4 mmol/L, Na 158 mmol/L, glucose 34 mmol/L, with osmolality now 371 ((2×158)+34+21=371 mosmol/kg).’

The patient doesn’t require as much oxygen as when she arrived, this can be reduced.

Prescribe (see Figs 6.4–6.6)

Oxygen, e.g. 40% OXYGEN via a FACE MASK

STOP

Initial oxygen prescription

Definitive Management [2]

Ongoing management of this patient should involve the inpatient specialist diabetes team, senior medical doctors, and HDU or ITU staff depending on the severity of the clinical condition

Frequent monitoring of clinical hydration status, GCS and fluid balance every 1–2 hours, particularly looking for overload (i.e. SOB, wet crackles in the chest, peripheral oedema) and cerebral oedema (suggested by reduced GCS)

Measure blood glucose, Na, K, and calculate osmolality every hour for the first 6 hours, then, if biochemistry is normalizing, 2-hourly for 6 hours

Aim to gradually drop osmolality by 3–8 mosmol/kg/h and achieve a positive fluid balance of 2–3 L at 6 hours, and 3–6 L at 12 hours. Guidelines also suggest reducing plasma sodium by no more than 10 mmol/L/day. Note that full biochemical normalization is unlikely to be achieved within 24 hours

Insulin as a fixed rate intravenous insulin infusion at 0.05 units/kg/h, can be started once the blood glucose is falling at less than 5 mmol/L/h with adequate fluid balance. Adjust at 1 unit/h to achieve a target glucose between 10 and 15 mmol/L in the presence of adequate positive fluid balance

IV fluids against fluid balance: Increase the rate of IV fluids if target for positive balance is not met. If the osmolality is no longer declining despite adeqate fluid replacement with 0.9% sodium chloride, AND an adequate rate of fall of plasma glucose is not being achieved, then 0.45% sodium chloride should be used instead of 0.9% sodium chloride

Glucose replacement: If blood glucose falls below 14 mmol/L prescribe additional 10% glucose at 125 mL/h

Continue to treat and monitor for resolution of precipitant: In this case, the lobar pneumonia

Protect and monitor feet: There is a high risk of pressure ulceration. Apply heel protectors if patient is at high risk, e.g. obtunded with known peripheral neuropathy

Follow-on care: Once the patient is biochemically normal, eating and drinking, the insulin infusion can be discontinued (if started) and regular oral hypoglycaemics and/or SC insulin started. This should be in liaison with the diabetes team.

Handing over the Patient

’69-year-old Mrs Jones has hyperosmolar hyperglycaemic state, with a background of Type 2 diabetes, normally diet controlled. She’s hypovolaemic and septic, secondary to a right lower lobe pneumonia.

Her sats were 85% when she came in, but went up to 100% on high-flow oxygen. I’ve now put her on 40% via a face mask. She responded well to a fluid bolus of 0.9% sodium chloride, and is currently having 1 L IV 0.9% sodium chloride over 2 hours, which will finish in an hour. The first doses of co-amoxiclav and clarithromycin have been given.

She’s currently on a monitored bed in MAU. Her admission FBC was Hb 134 g/L, WCC 16.7×10⁹/L, platelets 198×10⁹/L. Her U&Es and glucose were repeated an hour ago and they show urea 21 mmol/L, creatinine 165 μmol/L, K 3.4 mmol/L, Na 158 mmol/L, glucose 34 mmol/L, with osmolality now 371 mosmol/kg, which is down from 379 mosmol/kg on admission. Capillary ketones were only 0.3 mmol/L on arrival, so the patient hasn’t been treated as DKA.

Can you review her now to check her sats are adequate and repeat a VBG, U&Es and blood sugar. If she continues to respond so well she’s likely to be okay to go to the ward, but if she remains shocked or hypoxaemic consider discussing her with HDU.’

Station 6.3: Hypoglycaemia

You’re the junior doctor on shift in A&E resus with your registrar. A 16-year-old girl, Yasmin Grey, presents unconscious brought in by ambulance. Her accompanying friends tell you that they were at a party and 15 minutes before they found her she was ‘pretty drunk’ but seemed otherwise fine. An electronic discharge summary from 6 months ago states a new diagnosis of Type 1 diabetes.

Patient Details

Name:	Yasmin Grey
DOB:	15/05/1998
Hospital Number:	459023211
Weight:	50 kg (last admission)
Height:	164 cm (last admission)
Consultant:	Dr Taylor
Hospital/Ward:	WGH A&E
Current Medications:	Insulin aspart (Novorapid®) 9 units SC before breakfast/lunch/dinner, plus Insulin glargine (Lantus®) 26 units SC before dinner
Allergies:	Nil
Admission date:	02/02/14

Initial differential diagnosis for a coma [3]

Drugs:

Metabolic:

Hepatic encephalopathy

Endocrine:

Hypo- or hyperglycaemia

Severe hypothyroidism

Neurological:

Malignancy inc. metastases

Epilepsy/post-ictal state

Complications of hypoglycaemia

Confusion

Seizures

Focal neurological signs

Coma

Death

Prescribe (see Fig. 6.7)

Fluid challenge, e.g. 0.9% SODIUM CHLORIDE 500 mL IV (over 15 min)

IV glucose, e.g. 20% GLUCOSE 50 mL IV STAT

Figure 6.7

Hypoglycaemia management summary

Hypoglycaemia is an easily treatable medical emergency but, if unrecognized, can be fatal

First line treatment is IV glucose and follow-up with longer acting oral carbohydrates

Monitor blood sugar

Initial Assessment

Airway

Assess patency of the airway

She’s unconscious so at high risk of losing her airway. Vomiting is a particular risk given that she may have overdosed

‘There is no vomit or foreign material in the airway. There are obvious snoring noises audible.’

Your registrar asks you to apply a jaw thrust which relieves the airway noises. He asks the nurse to get an endotracheal tube ready, but asks you to maintain the jaw thrust for the time being.

Breathing

Check respiratory rate, oxygen saturations, work of breathing, and auscultate the chest. Respiratory rate and oxygen saturations could be affected by alcohol or drugs. There is a risk of aspiration

‘Respiratory rate is 15 breaths per minute. Saturations are 96% on air. The lung fields are clear to auscultation.’

No action required.

Circulation

Assess pulse, BP, CRT, and for other signs of dehydration or shock. Look particularly for hypertension and tachycardia, which could be caused by drugs

‘Yasmin is cool peripherally, with a HR of 110 bpm, BP of 120/80 mmHg, and CRT of 3 seconds.’

The patient is shocked and should be given a fluid challenge.

Disability

Assess GCS and blood sugar

‘The blood sugar is 1.1 mmol/L. Eyes open to painful stimuli (E2), there is moaning but no comprehensible words (V2), and arms flex to sternal pressure (M4): GCS 8/15.’

This patient is symptomatically hypoglycaemic and requires urgent treatment.

Exposure

Check temperature, this can be raised in overdoses of drugs such as ecstasy. Examine for evidence of self-harm. Look for evidence supporting other possible causes of reduced GCS, including infection. Check through possessions for other medications and recreational drugs

‘Temperature is 36.9°C. There is no evidence of previous or current self-harm.’

Initial Investigations

Bloods including U&Es, LFTs, clotting (many drugs cause hepatic and renal impairment, including paracetamol, a common drug in overdose), paracetamol and salicylate levels (overdoses can include more than one drug)

Venous blood gas: Confirmation of capillary blood glucose

Urine drug screen: This will look for amphetamines, benzodiazepines, cocaine, cannabis, ecstasy, opioids. This is particularly relevant if reduced consciousness persists or recurs despite treatment of hypoglycaemia

Alcohol breathalyser

ABG: Many drugs can alter acid–base status including paracetamol, alcohol, and salicylates.

Hypoglycaemia: when to treat and symptoms

A blood glucose≤3 mmol/L requires urgent action.

≤3=adrenergic symptoms:

sweating

flushing

palpitations.

≤2=neuroglycopaenic symptoms:

confusion

tiredness

focal neurological signs

reduced consciousness.

Causes of hypoglycaemia in Type 1 diabetes

This case is a good example of why a rigid approach to ABCD can occasionally lead to a loss of perspective and priority. This girl has a normal blood pressure (120/80) and urea. The tachycardic is due to her blood sugar of 1.3 mmol/L. She is young and will not die of dehydration but could be permanently damaged in minutes if she does not get any glucose. Therefore the IV glucose (under Disability) should be given before the fluid challenge (under Circulation).

Table 6.4

Yasmin’s blood results and ABG

Parameter	Value	Normal range (Units)
WCC	7×10⁹/L	4–11 (×10⁹/L)
Neutrophil	4×10⁹/L	2–7.5 (×10⁹/L)
Lymphocyte	2×10⁹/L	1.4–4 (×10⁹/L)
Platelet	200×10⁹/L	150–400 (×10⁹/L)
Haemoglobin	140 g/L	Men: 135–177 (g/L) Women: 115–155 (g/L)
PT	12 seconds	11.5–13.5 seconds
APTT	30 seconds	26–37 seconds
CRP	10 mg/L	<5 (mg/L)
Urea	6 mmol/L	2.5–6.7 (mmol/L)
Creatinine	80 μmol/L	79–118 (μmol/L)
Sodium	140 mmol/L	135–146 (mmol/L)
Potassium	4 mmol/L	3.5–5.0 (mmol/L)
eGFR	>60 mL/min	>60 (mL/min)
Bilirubin	7 μmol/L	<17 (μmol/L)
ALT	20 IU/L	<40 (IU/L)
ALP	100 IU/L	39–117 (IU/L)
Glucose	1.3 mmol/L	4.5–5.6 (mmol/L) (fasting)
Lactate	3 mmol/L	0.6–2.4 (mmol/L)
Paracetamol/salicylate levels	Undetectable	Undetectable
pH	7.30	7.35–7.45
PaO₂	12 kPa	10.6–13.3 (kPa) on air
PaCO₂	5 kPa	4.8–6.1 (kPa)
HCO₃	20 mmol/L	22–26 (mmol/L)

‘Initial bloods confirm hypoglycaemia with a blood sugar of 1.3 mmol/L. There is an associated CRP rise of 10 mmol/L, with a lactate of 3 mmol/L. Blood gas shows a metabolic acidosis. Breathalyser shows low levels of alcohol in the bloodstream, urine toxicology is negative, and paracetamol/salicylate levels are undetectable.’

Initial Management [4]

Airway: If consciousness level does not improve rapidly with treatment of hypoglycaemia the patient will need a definitive airway

Hypoglycaemia treatment: In conscious patients, oral glucose or sweet drinks can be used. IV glucose is used for patients with reduced consciousness; 50 mL of 20% glucose, or 160 mL of 10% glucose can be used; 50% glucose is not recommended due to the heightened risk of extravasation injury compared with less concentrated solutions. If given, it should be given into a large vein through a large-gauge needle

1 mg of glucagon IM/SC/IV is an alternative, particularly in out of hospital settings, or in hospital situations if there is difficult IV access. Glucagon is ineffective in those with low glycogen stores (e.g. malnourished patients) [4], and can cause gastrointestinal side effects including nausea, vomiting and abdominal pain.

Reassessment

‘After about 5 minutes Yasmin started to move around and groan, and sat up on the trolley. Five minutes later she was able to talk and could make orientated conversation. She says she drunk a bottle of wine at the party and hasn’t really drunk that much before. Also she injected herself with her normal dose of insulin at dinner time, but ate very little.’

Hypoglycaemia in this case is likely multifactorial due to her insulin administration despite her missed meal and heavy alcohol consumption (alcohol inhibits gluconeogenesis).

Definitive Management

Regular ABCDE assessment, including capillary blood glucose needs to be continued, as there is a risk she’ll become hypoglycaemic again, particularly if she had injected a long-acting insulin

Replenish glycogen stores: The patient needs to eat a meal containing carbohydrate, e.g. two slices of toast

Complete history is now needed to determine the type of insulin injected, the dose injected and timing. Also check if any recreational drugs were taken

Counselling before discharge about compliance with diabetic medications, the importance of adjusting insulin when meal size varies, and trying to avoid binge-drinking

In cases of hypoglycaemia with no obvious precipitant, blood samples for insulin and c-peptide should be taken. If c-peptide levels are high this suggests increased endogenous insulin production, i.e. an insulinoma.

Handing over the Patient

‘Yasmin Grey is a 16-year-old girl with Type 1 diabetes who presented unconscious with a GCS of 8 on arrival and capillary blood glucose of 1.3 mmol/L. After giving IV glucose she regained full consciousness, and is now back to her normal self and has eaten some toast.

Please repeat capillary blood glucose and neuro observations hourly overnight. If she’s well in the morning she can be discharged. Can you please ensure she’s referred to the inpatient diabetic nurse specialists for counselling and education before she goes.’

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Tags: The Unofficial Guide to Prescribing

Nov 18, 2017 | Posted by admin in PHARMACY | Comments Off

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Endocrinology

Endocrinology

Station 6.1: Diabetic ketoacidosis

Initial Assessment

Airway

Breathing

Circulation

Disability

Exposure

Initial Investigations

Initial Management [1]

Reassessment

Definitive Management [1]

Handing over the Patient

Station 6.2: Hyperosmolar hyperglycaemic state (HHS)

Initial Assessment

Airway

Breathing

Circulation

Disability

Exposure

Initial Investigations

Initial Management [2]

IV fluids

Reassessment

Definitive Management [2]

Handing over the Patient

Station 6.3: Hypoglycaemia

Initial Assessment

Airway

Breathing

Circulation

Disability

Exposure

Initial Investigations

Initial Management [4]

Reassessment

Definitive Management

Handing over the Patient

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