Uncategorized - Nurses Revision

Ovarian Cysts: Recognition, Assessment and Emergency Management

Why this topic matters: Ovarian cysts are common and often benign, but a cyst may twist the ovary, rupture, bleed or become infected. Sudden unilateral pelvic pain with nausea/vomiting is an ovarian-torsion emergency until proven otherwise. A positive pregnancy test changes the differential to ectopic pregnancy, and postmenopausal or complex masses require careful malignancy assessment. Emergency medical technicians must stabilise first, test pregnancy, control pain, identify shock and obtain urgent gynaecology review.

Learning objectives

Define functional and pathological ovarian cysts and explain torsion, rupture and haemorrhage.
Recognise chronic pressure symptoms and acute cyst accidents.
Perform ABCDE, pregnancy testing, focused pelvic history, examination and initial investigations.
Describe emergency care for torsion, rupture, haemorrhage, infection and suspected malignancy.
Plan nursing monitoring, referral, fertility discussion, discharge safety-netting and prevention of delayed care.

Anatomy and definition

The ovaries lie on either side of the uterus and release ova and sex hormones. An ovarian cyst is a fluid-filled, solid or mixed lesion arising from or near the ovary. Functional cysts form during normal ovulation and often resolve; pathological cysts include endometriomas, dermoid/teratoma, cystadenoma, inflammatory masses and malignant tumours.

The term ovarian cyst accident describes an acute complication such as torsion, rupture or haemorrhage. RCOG guidance emphasises considering these complications when a patient with an ovarian mass presents with acute pain.

Types and risk settings

Type	Characteristics	Emergency relevance
Functional follicular/corpus luteum	Often related to ovulation; usually simple and self-limiting.	May rupture, bleed or act as a lead point for torsion.
Endometrioma	Old blood associated with endometriosis; chronic pelvic pain/infertility.	Rupture causes acute pain and peritoneal irritation; torsion is possible.
Dermoid/teratoma	Benign germ-cell tumour containing fat or calcification.	Common torsion risk; rare rupture/infection.
Polycystic ovaries	Multiple follicles within a hormonal syndrome; not the same as a single large cyst.	Do not label acute pain as PCOS without evaluating emergencies.
Complex or solid mass	Septations, papillary projections, solid areas, ascites or bilateral disease.	Needs specialist assessment for malignancy or advanced disease, especially after menopause.

Clinical presentations

Many cysts are asymptomatic and found incidentally on ultrasound.
Pressure symptoms include pelvic fullness, bloating, urinary frequency, constipation, dyspareunia or early satiety.
Hormonal activity may cause irregular, heavy or painful periods.
Sudden severe unilateral pain, nausea and vomiting suggest torsion; pain may be intermittent when the ovary twists and untwists.
Sudden pain after exertion or intercourse may follow rupture; dizziness, pallor, syncope or shock suggests intra-abdominal bleeding.
Fever, worsening pain, offensive discharge or sepsis may indicate infection/abscess or another pelvic source.

Emergency red flags: sudden severe unilateral pelvic pain, persistent vomiting, syncope, pallor, hypotension, tachycardia, abdominal guarding, positive pregnancy test, fever, rapidly increasing abdominal distension, shoulder-tip pain, heavy bleeding or an acute abdomen in a postmenopausal patient.

First contact and scene priorities

Provide privacy, introduce yourself and explain that acute pelvic pain has several urgent causes. Obtain consent before sensitive questions or examination.
Assess ABCDE and activate emergency transport/gynaecology support for shock, peritonism, pregnancy, torsion or uncontrolled pain.
Ask for last menstrual period, pregnancy possibility, contraception, previous cyst/endometriosis, fertility treatment, surgery and medicines.
Keep a potentially operative patient nil by mouth after senior review; provide analgesia and antiemetic without delaying diagnosis.
Do not reassure because a cyst was previously labelled “benign”; a new torsion, rupture or ectopic pregnancy can occur.

ABCDE assessment

A — Airway

Assess vomiting, reduced consciousness, aspiration risk and opioid effect after analgesia.
Provide airway support as trained if shock, bleeding or sedation compromises protection.

B — Breathing

Measure respiratory rate and SpO₂; assess pain-related splinting, aspiration, pulmonary embolism and severe anaemia.
Give oxygen for hypoxaemia or distress and prepare for urgent transfer.

C — Circulation

Check pulse, BP, capillary refill, skin, bleeding and signs of internal haemorrhage or sepsis.
Obtain IV access, take blood for full count, group/crossmatch, electrolytes, renal function and pregnancy testing.
Give isotonic crystalloid for hypovolaemia under local protocol and reassess after every bolus.

D — Disability

Record AVPU/GCS, glucose, syncope, dizziness and severe pain-related distress.
Altered consciousness with pelvic pain is shock/haemorrhage or another serious condition until proven otherwise.

E — Exposure

Inspect for pallor, distension, scars, bruising, vaginal bleeding, fever and signs of infection while preserving dignity.
Perform abdominal and, when indicated, pelvic examination with consent, chaperone and trained staff.

Focused history

History area	Questions	Clinical value
Pain	Onset, sudden/gradual, side, severity, radiation, constant/intermittent, after sex/exercise and previous episodes.	Suggests torsion, rupture, haemorrhage, ectopic or appendicitis.
Pregnancy	LMP, contraception, pregnancy possibility, fertility treatment, miscarriage/ectopic history.	Changes diagnosis, imaging and treatment urgently.
Associated symptoms	Nausea/vomiting, fever, discharge, urinary/bowel symptoms, dizziness, fainting or shoulder pain.	Assesses torsion, infection, internal bleeding and obstruction.
Mass history	Previous ultrasound size/appearance, growth, bilateral disease, endometriosis, family cancer history.	Guides benign vs complex/malignant referral.
Medication/surgery	Anticoagulants, fertility medicines, hormonal treatment, previous pelvic surgery.	Identifies bleeding/torsion risk and operative considerations.

Differential diagnosis of acute pelvic pain

Condition	Clues	Immediate response
Ovarian torsion	Sudden intermittent unilateral pain with nausea/vomiting; adnexal mass risk.	Urgent gynaecology and operative assessment; do not wait for a “perfect” ultrasound.
Rupture/haemorrhage	Sudden pain, free fluid, pallor, syncope, falling haemoglobin or shock.	IV access, fluids/blood pathway, crossmatch and surgical review.
Ectopic pregnancy	Positive pregnancy test, unilateral pain, bleeding, shoulder pain or collapse.	Pregnancy emergency pathway and urgent surgery/gynaecology.
PID/abscess	Fever, discharge, cervical/adnexal tenderness and sepsis.	Pregnancy test, antibiotics and admission/referral when severe.
Appendicitis/renal colic	Right-sided pain, urinary symptoms, haematuria, fever or bowel signs.	General surgical/renal assessment and targeted imaging.

Investigations

Urine/serum pregnancy test in every patient of reproductive potential with pelvic pain or bleeding.
Full blood count for anaemia/infection; group and crossmatch if bleeding or surgery is possible; CRP, electrolytes, renal/liver function and urinalysis as indicated.
Pelvic ultrasound with Doppler is first-line in many settings for cyst morphology, free fluid, pregnancy and torsion assessment. Normal Doppler flow does not reliably exclude torsion because intermittent or dual blood supply may persist.
CT/MRI is selected by the specialist team for complex mass, malignancy, bowel/urinary complications or uncertain diagnosis.
In postmenopausal or complex lesions, specialist tumour-marker and oncology pathways may be needed; do not interpret CA-125 alone as proof of cancer or benign disease.

Management of suspected ovarian torsion

Treat sudden unilateral pain with nausea/vomiting as torsion until proven otherwise and call gynaecology urgently.
Keep nil by mouth, provide IV access, analgesia/antiemetic, fluids if dehydrated and repeated vital signs.
Do not delay referral for prolonged outpatient observation or repeated imaging when clinical suspicion is high; ovarian blood supply is time-sensitive.
Definitive treatment is usually urgent laparoscopy to detorse and preserve the ovary when viable; cystectomy or oophorectomy is decided by the surgical team.
After surgery, monitor pain, bleeding, fever, urine output, wound and fertility concerns; provide emotional support.

Management of rupture or haemorrhage

Assess shock and internal bleeding; lie the patient safely, keep warm, obtain IV access and use haemorrhage protocols.
Send full blood count, group/crossmatch and serial haemoglobin; monitor lactate, urine output, abdominal signs and response to fluids.
Stable patients may be observed with analgesia and serial imaging under specialist care; unstable patients require urgent operative/interventional management.
Consider pregnancy/ectopic pregnancy, anticoagulants, bleeding disorders and trauma rather than assuming a simple cyst rupture.

Management of uncomplicated or persistent cysts

Many simple functional cysts resolve; follow-up ultrasound and gynaecology review are based on size, appearance, age, symptoms and menopausal status.
Persistent, enlarging, complex, bilateral or symptomatic masses need specialist assessment, sometimes surgery or oncology referral.
Oral contraceptives do not reliably make an existing cyst disappear, though hormonal therapy may be used for related menstrual/endometriosis symptoms.
Discuss fertility, ovarian reserve, risks of surgery and shared decision-making before elective cystectomy or oophorectomy.

Nursing and EMT interventions

Trend pain, pulse, BP, temperature, bleeding, abdominal signs, urine output and response to analgesia/fluids.
Maintain nil-by-mouth status when operation is likely; document last food/drink and allergies.
Monitor IV site, antiemetic/opioid sedation, fluid overload, haemoglobin trend and signs of sepsis.
Provide privacy, a chaperone and clear explanations for pelvic examination, ultrasound and surgery.
Use teach-back for return precautions: worsening unilateral pain, vomiting, fever, faintness, heavy bleeding, distension or positive pregnancy test.

Prevention and follow-up

Attend planned ultrasound/gynaecology follow-up for cysts that are complex, persistent, large or symptomatic.
Seek emergency care for sudden severe pain with vomiting or faintness rather than self-treating for several days.
Discuss fertility treatment risks, especially ovarian stimulation and ovarian hyperstimulation syndrome, with the fertility team.
Maintain a pain/menstrual diary and review recurrent cysts, endometriosis, contraception and family cancer history.
Use safe analgesics and avoid excess NSAIDs when pregnant, anticoagulated, ulcer-prone or renally impaired.

Clinical scenarios

Scenario 1 — Torsion: A 17-year-old has sudden intermittent left pelvic pain, vomiting and a known dermoid cyst. Her vitals are currently stable. Give analgesia/antiemetic, pregnancy test, IV access, keep nil by mouth and arrange urgent gynaecology review; normal initial Doppler flow must not falsely reassure the team.

Scenario 2 — Rupture with shock: A woman collapses after sudden lower-abdominal pain and is pale, tachycardic and hypotensive. Treat as internal haemorrhage/ectopic until proven otherwise: ABCDE, oxygen if indicated, large-bore IV access, crossmatch, cautious resuscitation, urgent imaging/surgery and continuous reassessment.

Scenario 3 — Postmenopausal mass: A 61-year-old has progressive bloating, early satiety and a complex bilateral mass. She is stable but anaemic. Arrange urgent gynaecology/oncology assessment and investigate anaemia; do not label it a simple functional cyst.

Common errors to avoid

Failing to perform a pregnancy test or missing ectopic pregnancy.
Delaying torsion surgery because pain is intermittent or Doppler flow is present.
Assuming every cyst is benign, especially after menopause or with complex morphology.
Giving repeated analgesics without monitoring shock, bleeding, vomiting, renal function or opioid sedation.
Discharging a patient with syncope, guarding, persistent vomiting, fever or uncontrolled pain.

CYST SAFE: C — Circulation/ABCDE; Y — Young/reproductive pregnancy test; S — Sudden unilateral pain = torsion; T — Test blood and ultrasound; S — Shock/bleeding protocol; A — Analgesia/antiemetic; F — Fast gynaecology referral; E — Explain follow-up and return signs.

Revision questions

Differentiate functional, endometrioma, dermoid and complex ovarian cysts.
What symptoms suggest torsion, rupture, haemorrhage or infection?
Why is a pregnancy test essential in acute pelvic pain?
Why does normal Doppler flow not completely exclude torsion?
Outline the management of the shocked patient in Scenario 2.
Which cyst features require specialist or oncology referral?

Key takeaways

An ovarian cyst becomes an emergency when it twists, ruptures, bleeds, infects or masks another life-threatening diagnosis. Stabilise ABCDE, test pregnancy, treat pain and shock, refer suspected torsion urgently and never let a previous “benign cyst” label delay reassessment.

References for further study

Royal College of Obstetricians and Gynaecologists. Management of suspected ovarian masses in premenopausal women.
NHS. Ovarian cyst — symptoms and urgent warning signs.
ACOG. Adnexal torsion in adolescents.
NICE Clinical Knowledge Summaries. Acute abdominal pain: gynaecological causes.
Follow current Uganda Ministry of Health and specialist gynaecology protocols for pelvic pain, torsion, haemorrhage and ovarian masses.

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Sexual Violence: Survivor-Centred Emergency Assessment, Care and Referral

Why this topic matters: Sexual violence is a medical, psychological, public-health and human-rights emergency. A survivor may present with injuries, pregnancy risk, sexually transmitted infection (STI) exposure, HIV exposure, intoxication, suicidal thoughts or no visible injury at all. Emergency providers must protect immediate safety, listen without judgement, obtain informed consent for each step, treat injuries, offer time-sensitive prophylaxis, preserve evidence when the survivor wants it, document accurately and link the person to protection, psychosocial, legal and follow-up services.

Survivor-centred principle: The survivor controls disclosure and examination as far as safety and applicable law permit. Do not blame, pressure, repeatedly question, promise a legal outcome or make care conditional on reporting to police. Follow current Uganda Ministry of Health, child-protection, forensic and mandatory-reporting requirements.

Learning objectives

Define sexual violence and explain the immediate medical, psychological, reproductive, infectious and safety consequences.
Use WHO first-line support (LIVES) and trauma-informed communication from first contact to discharge.
Perform ABCDE, injury assessment, pregnancy/STI/HIV risk assessment and suicide/safeguarding screening.
Describe emergency contraception, HIV PEP, STI/hepatitis B/tetanus care, wound management and referral.
Document objectively, preserve evidence with consent, maintain confidentiality and coordinate multidisciplinary follow-up.

Definition and forms of sexual violence

Sexual violence includes any sexual act, attempt to obtain a sexual act, unwanted sexual comments or advances, or acts directed against a person’s sexuality using coercion, intimidation, force, abuse of power, incapacity or inability to consent. It may occur in or outside intimate relationships and can affect women, men, children, adolescents, people with disabilities and people of any sexual orientation or gender identity.

Examples include rape, attempted rape, sexual assault, unwanted touching, forced sexual acts, sexual exploitation, trafficking, forced marriage, reproductive coercion, technology-facilitated sexual abuse and abuse of a child. The emergency response is based on safety, health needs and consent—not on the survivor’s clothing, relationship, previous sexual activity, alcohol use or decision to report.

Potential consequences

Domain	Possible consequences	Emergency questions
Physical injury	Bleeding, genital/anal tears, bruises, strangulation injury, fractures, head injury, burns or abdominal trauma.	Airway, breathing, shock, neck pain, dysphonia, dysphagia, neurological deficit and severe pain.
Pregnancy/reproductive	Unintended pregnancy, miscarriage, genital injury, infertility or reproductive coercion.	Last menstrual period, pregnancy possibility, bleeding, abdominal pain and emergency contraception time window.
Infection	HIV, gonorrhoea, chlamydia, trichomonas, syphilis, hepatitis B and other infections.	Exposure type, mucosal injury, time since assault, source information and vaccination status.
Psychological	Acute stress, fear, shame, dissociation, anxiety, depression, PTSD, substance use and suicidal thoughts.	Immediate safety, self-harm plan, safe place, perpetrator access and supportive person.
Social/legal	Threats, retaliation, homelessness, stigma, family conflict, school/work disruption and legal concerns.	Safe discharge, child protection, disability support, shelter and confidential referral.

First contact: privacy, safety and consent

Move the survivor to a private, quiet, secure space away from the alleged perpetrator, relatives who may pressure them and unnecessary observers.
Introduce yourself, explain your role and ask how the person wishes to be addressed. Offer a trained interpreter, chaperone and support person chosen by the survivor when safe.
Explain that medical care, evidence collection, reporting and counselling are separate choices. Obtain consent before history, examination, photographs, specimens, treatment and information sharing.
Ask only what is needed for immediate care first. Do not conduct an investigative interrogation or ask “why” questions that imply blame.
Assess whether the survivor is safe to return home. If the alleged perpetrator or a dangerous household member has access, involve safeguarding/protection services.

WHO LIVES first-line support

Letter	Action	Practical language
L — Listen	Listen actively, patiently and privately; do not interrupt or demand details.	“I’m listening. You can tell me only what you feel able to share.”
I — Inquire about needs	Ask about physical injuries, emotional distress, safety, pregnancy/STI concerns and urgent practical needs.	“What worries you most right now? Are you safe to leave here?”
V — Validate	Believe, affirm and remove blame without promising a legal result.	“I’m sorry this happened. It was not your fault.”
E — Enhance safety	Plan immediate safety, protection, shelter, transport and risk reduction.	“Who can safely support you today?”
S — Support and refer	Offer medical treatment, psychosocial care, legal/forensic and social referrals according to choice and law.	“We can explain your options and support whichever safe choice you make.”

ABCDE emergency assessment

A — Airway

Assess voice change, difficulty swallowing, neck pain, facial injury and strangulation. Airway swelling can worsen after a delay.
Call for advanced airway help if there is respiratory distress, cyanosis, reduced consciousness or suspected neck injury.

B — Breathing

Measure respiratory rate and SpO₂; look for chest trauma, aspiration, poisoning or strangulation-related hypoxia.
Give oxygen for hypoxaemia/distress, provide ventilation support as trained and monitor closely after strangulation even when initial findings are mild.

C — Circulation

Assess pulse, BP, capillary refill, skin, bleeding, abdominal tenderness and shock. Control external haemorrhage with gentle direct pressure.
Establish IV access for major injury, bleeding, severe pain, poisoning or shock; take blood tests/crossmatch as clinically indicated.
Give isotonic fluid or blood products according to the trauma/haemorrhage protocol, while preserving evidence and dignity.

D — Disability

Record AVPU/GCS, pupils, glucose, seizures, head injury, intoxication and suicidal thoughts.
Do not assume altered behaviour is consent, intoxication or “hysteria”; treat hypoxia, hypoglycaemia, head injury, overdose and shock.

E — Exposure and examination

Expose only the area being examined, use warm coverings and explain each step. Look for bruises, ligature marks, tears, burns, bite marks and other injuries.
Examine genital/anal areas only with consent and trained staff; emergency stabilisation always takes priority.

Essential history without re-traumatisation

Time and safety: When did it happen? Is the alleged perpetrator nearby or threatening the survivor now?
Exposure: What type of contact occurred, including vaginal, anal or oral exposure, ejaculation, condom use, mucosal injury, force, weapons, restraint or drug/alcohol facilitation? Ask neutrally and accept “I don’t know.”
Symptoms: Pain, bleeding, dysuria, discharge, abdominal pain, headache, neck pain, breathing/voice change, vomiting or loss of consciousness.
Pregnancy: Last menstrual period, contraception, pregnancy possibility, pregnancy intention and previous pregnancy.
Medical history: HIV status, medicines, allergies, hepatitis B vaccination, tetanus status, bleeding disorders, diabetes, mental health and current treatment.
Evidence: Has the survivor bathed, changed clothes, urinated, eaten, brushed teeth or washed the mouth? Ask sensitively; do not blame or withhold care if these occurred.
Support: Who can safely accompany the survivor? What are their immediate safety, shelter, transport, financial and child-care needs?

Injury examination and treatment

Perform a head-to-toe examination with consent, documenting size, shape, colour, location, tenderness and function of each injury.
Assess strangulation carefully: voice change, neck pain, swallowing difficulty, petechiae, facial swelling, neurological symptoms or loss of consciousness require urgent senior review and observation/imaging.
Clean and close wounds according to trauma principles; assess tetanus status and provide prophylaxis when indicated.
Provide analgesia, antiemetics, wound care and treatment of fractures/burns. Avoid unnecessary genital cleansing before forensic examination if the survivor wants evidence collection.
Consider intoxication, drug-facilitated assault and overdose; maintain airway, check glucose and obtain toxicology only with consent/policy.

Pregnancy prevention and pregnancy care

Offer emergency contraception as soon as possible when pregnancy is possible and not desired. WHO post-rape care indicators recognise emergency contraception for survivors who present within five days; follow the locally available option and product instructions.
Perform pregnancy testing when appropriate, remembering a very early test may be negative. Arrange repeat testing and follow-up if menstruation is delayed.
If pregnancy results from assault, provide non-directive counselling, obstetric care, psychosocial support and information on legally available options under Ugandan law.
Do not withhold contraception or HIV/STI care because the survivor is considering reporting, abortion care or continuing the pregnancy.

HIV, STI and hepatitis prevention

Need	Emergency action	Teaching point
HIV PEP	Risk-assess exposure and start an approved antiretroviral PEP regimen as soon as possible; CDC notes PEP should begin within 72 hours and is taken for the prescribed course, commonly 28 days.	Do not delay the first dose while waiting for source testing; arrange adherence and follow-up.
STI prevention	Offer empiric treatment for likely gonorrhoea, chlamydia and trichomonas according to current Uganda protocol and patient factors.	Explain side effects, abstinence/barrier protection during treatment and test-of-cure/follow-up when indicated.
Hepatitis B	Check vaccination/immunity and offer vaccine ± immunoglobulin according to exposure, source and national protocol.	Document dose and schedule; do not assume childhood vaccination is complete.
Testing	Baseline HIV, syphilis, pregnancy and other tests with consent; repeat at recommended intervals.	A negative early test does not exclude later infection; keep results confidential.

Forensic evidence and documentation

Explain the purpose, process and limits of forensic examination; obtain specific consent for each specimen and photograph. The survivor may accept medical care but decline evidence collection.
Document the survivor’s words in quotation marks where possible, including uncertainty; record date/time, who was present, findings, treatment, referrals and consent/refusal.
Use body maps and objective descriptions; avoid conclusions such as “mucosa proves rape” or “no injury means no assault.” Absence of injury does not disprove sexual violence.
Preserve clothing/specimens in labelled paper bags according to local chain-of-custody policy. Record collector, date/time, seal and transfer; never leave evidence unattended.
Do not delay life-saving care for evidence collection. If the survivor has washed or changed, provide care and document what was reported.
Share information only with consent or when a specific legal safeguarding duty applies; follow Ugandan policy for children, imminent danger and mandatory reporting.

Mental health, suicide and safeguarding

Ask directly and privately about fear, dissociation, self-harm thoughts, suicide plan, access to means, threats and ability to remain safe.
Provide psychological first aid, grounding, calm communication and a safe companion; avoid forced detailed recounting.
Urgently involve mental-health and safeguarding teams for suicidal intent, psychosis, severe dissociation, child abuse, trafficking, disability-related dependence or ongoing perpetrator access.
Make a written safety plan: safe place, emergency contacts, transport, phone privacy, medication/means safety and follow-up appointment.

Children and adolescents

Prioritise immediate safety, safeguarding and child-protection referral. Use age-appropriate language and explain confidentiality limits before disclosure.
Obtain assent from the child and consent from the legally appropriate guardian according to Ugandan law and facility policy; do not force the child to face the alleged perpetrator.
Use trained paediatric/forensic staff. Avoid repeated interviews and unnecessary examinations; coordinate a single multidisciplinary approach.
Assess injuries, pregnancy risk, STI/HIV exposure, tetanus/hepatitis B, developmental needs, school safety and caregiver reliability.

Discharge, referral and follow-up

Confirm that injuries are treated, vital signs stable, pain controlled, pregnancy/PEP/STI options explained and the survivor understands medicines.
Provide written dates for PEP refills, repeat HIV/STI/pregnancy tests, hepatitis B doses, wound review and mental-health follow-up.
Link to a trained counsellor, social worker, GBV protection service, legal/forensic service and safe shelter when desired.
Arrange safe transport and a confidential contact method. Do not call a number that the alleged perpetrator monitors.
Give return precautions: heavy bleeding, worsening pain, fever, vomiting, rash/medicine reaction, breathlessness, suicidal thoughts, new neurological symptoms or unsafe home situation.

Nursing and EMT responsibilities

Use a private survivor-centred room; limit staff access and protect records from unnecessary disclosure.
Maintain a calm, non-judgemental tone; offer choices and explain delays, examinations, medicines and referrals.
Monitor airway, circulation, pain, bleeding, neurological status, sedation, allergic reaction and psychological distress.
Double-check PEP/STI/EC medicines, allergies, pregnancy status, renal/hepatic considerations and follow-up schedule.
Document objective findings and every consent/refusal; preserve chain of custody where evidence is collected.
Use team debriefing and supervision after difficult cases while maintaining survivor confidentiality.

Clinical scenarios

Scenario 1 — Recent assault, stable survivor: A 22-year-old presents 10 hours after rape, distressed but haemodynamically stable. Provide privacy and LIVES, assess injuries and pregnancy risk, obtain consent, offer EC, HIV PEP and STI/hepatitis care according to Uganda protocol, document objectively, offer evidence collection and arrange safe follow-up. Reporting is explained as an option/obligation only where applicable by law, not a condition for care.

Scenario 2 — Strangulation: A survivor has hoarseness, neck tenderness and brief loss of consciousness but normal SpO₂. Treat as a potentially delayed airway/vascular injury: ABCDE, urgent senior/trauma review, observation and imaging according to protocol. Do not discharge because there are no external marks.

Scenario 3 — Child survivor: An 11-year-old is brought by a caregiver and gives a brief disclosure. Ensure privacy and safety, use child-protection procedures, obtain appropriate consent/assent, avoid repeated questioning and coordinate paediatric, forensic, psychosocial and legal services.

Common errors to avoid

Blaming the survivor, asking “why” questions, doubting disclosure or making care dependent on police reporting.
Missing strangulation, head injury, pregnancy, HIV exposure, poisoning, severe bleeding or suicide risk.
Performing an examination or taking specimens without informed consent or an appropriate chaperone.
Assuming no visible injury means no assault or that a survivor who washed has no right to care/evidence discussion.
Failing to start time-sensitive HIV PEP/EC because test results or a police form is unavailable.
Discharging to an unsafe home or sharing confidential information with a person who may be involved.

SAFE CARE: S — Safety and privacy; A — ABCDE and injuries; F — First-line LIVES support; E — Explain consent/options; C — Contraception, HIV PEP, STI/hepatitis care; A — Accurate documentation/evidence; R — Referral and safe discharge; E — Emotional/suicide/safeguarding assessment.

Revision questions

What does LIVES stand for, and why is it appropriate for every survivor?
List the immediate medical priorities after sexual violence.
Why must strangulation be treated as an emergency even when external marks are absent?
What are the time-sensitive options for pregnancy and HIV prevention?
Which documentation and chain-of-custody principles protect the survivor and the case?
How should the approach differ for a child or adolescent survivor?
Write an SBAR handover for Scenario 2.

Key takeaways

Believe, protect, treat and support. Stabilise injuries first, provide LIVES first-line support, obtain consent, offer pregnancy/STI/HIV prevention promptly, preserve evidence only with consent, assess safety and suicide risk, and arrange confidential multidisciplinary follow-up.

References for further study

WHO. Clinical management of rape and intimate partner violence, 2024 training package.
WHO. Responding to intimate partner violence and sexual violence against women: clinical and policy guidelines.
CDC. Sexual Assault and Abuse and STIs: STI Treatment Guidelines.
CDC. HIV Post-Exposure Prophylaxis — start as soon as possible and within 72 hours.
Follow current Uganda Ministry of Health GBV/clinical management of rape, child-protection, forensic and PEP/EC protocols.

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Endometriosis: Recognition, Assessment and Emergency Management

Why this topic matters: Endometriosis is an oestrogen-dependent inflammatory condition in which tissue similar to endometrium grows outside the uterine cavity. It commonly causes cyclical pelvic pain, painful periods, pain during sex, bowel/bladder symptoms and infertility. Most care is planned, but emergency providers must recognise acute complications such as ruptured endometrioma, ovarian torsion, bowel or urinary obstruction, severe haemorrhage, infection, ectopic pregnancy and uncontrolled pain. Severe menstrual or pelvic pain should never be dismissed as “normal.”

Learning objectives

Define endometriosis, describe common sites and explain inflammatory pain, adhesions and infertility.
Take a sensitive menstrual, reproductive, pain, bowel, bladder and sexual history.
Differentiate chronic endometriosis pain from ectopic pregnancy, torsion, appendicitis, pelvic infection and other acute abdomen emergencies.
Perform ABCDE, pregnancy testing, focused examination, analgesia, safe referral and emergency stabilisation.
Describe medical, hormonal, surgical, fertility, nursing and prevention-support strategies.

Definition and disease process

Endometriosis is the presence of endometrial-like glands and stroma outside the uterine cavity, commonly on the ovaries, pelvic peritoneum, uterosacral ligaments, bowel or bladder. Lesions respond to hormonal cycling, causing repeated inflammation, bleeding, fibrosis and adhesion formation. Endometriomas (“chocolate cysts”) contain old blood within the ovary.

Endometriosis is chronic and can recur. It is not cancer, but it can substantially affect education, work, relationships, sexual health, mental health and fertility. WHO notes that symptoms can be treated with medicines and, in some patients, surgery; diagnosis may use ultrasound and sometimes laparoscopy, but treatment should not be withheld simply because surgery has not yet confirmed the disease.

Common locations and clinical effects

Location	Possible symptoms	Emergency concern
Ovary/endometrioma	Unilateral pelvic pain, deep dyspareunia, infertility, pelvic mass.	Torsion, rupture, haemoperitoneum or acute severe pain.
Pelvic peritoneum/adhesions	Cyclical pelvic pain, chronic tenderness, reduced mobility of organs.	Adhesional bowel obstruction or acute abdomen from another cause.
Bowel/rectum	Painful defecation, cyclical constipation/diarrhoea, rectal bleeding, bloating.	Obstruction, perforation or significant bleeding is rare but urgent.
Bladder/ureter	Cyclical dysuria, haematuria, flank pain or urinary frequency.	Obstruction, hydronephrosis, infection or renal injury.
Thorax/diaphragm (rare)	Cyclical chest/shoulder pain, breathlessness or haemoptysis.	Catamenial pneumothorax or haemothorax requires emergency assessment.

Symptoms and impact

Severe dysmenorrhoea, pelvic or lower-back pain that begins before menstruation and lasts through the period.
Deep pain during or after sexual intercourse, vulvovaginal pain or fear of examination.
Painful bowel movements, cyclical diarrhoea/constipation, bloating or blood in stool.
Painful urination, urinary frequency or cyclical haematuria.
Heavy or irregular bleeding, fatigue, anaemia, infertility or difficulty conceiving.
Chronic pain sensitisation, sleep disturbance, anxiety, depression, reduced school/work attendance and relationship distress.

Emergency red flags: sudden unilateral severe pelvic pain, syncope, pallor, shock, shoulder-tip pain, positive pregnancy test, fever with guarding, persistent vomiting, abdominal distension, inability to pass urine/stool, haematuria, significant rectal/vaginal bleeding, breathlessness or haemoptysis.

First contact and compassionate communication

Provide privacy, introduce yourself, ask the patient’s preferred name and explain every step. Severe pelvic pain is real and deserves assessment.
Obtain consent before abdominal, pelvic, rectal or sexual-health questions/examination. Offer a chaperone and same-gender clinician when available.
Assess ABCDE and pain severity before taking a long history. Activate emergency referral for shock, peritonism, ectopic pregnancy or torsion.
Ask about pregnancy possibility, last menstrual period, contraception, fertility intentions, bleeding and previous endometriosis/endometrioma surgery.
Do not assume cyclical pain is benign; do not allow a known endometriosis label to obscure a new emergency.

ABCDE assessment

A — Airway

Assess responsiveness, vomiting, aspiration risk and need for analgesia/sedation monitoring.
Provide airway support if shock, haemorrhage, opioid use or reduced consciousness is present.

B — Breathing

Measure respiratory rate and SpO₂. Assess sudden breathlessness, pleuritic pain or haemoptysis for pulmonary embolism or rare thoracic endometriosis complications.
Give oxygen for hypoxaemia or respiratory distress and arrange urgent imaging/referral.

C — Circulation

Check pulse, BP, capillary refill, skin colour, temperature, urine output and signs of haemorrhage or sepsis.
Establish IV access in severe pain, bleeding, shock, suspected ectopic pregnancy, torsion or sepsis; take blood for full count, group/crossmatch and chemistry.
Give isotonic fluid for hypovolaemia under local protocol and reassess after each bolus.

D — Disability

Record AVPU/GCS and assess collapse, severe pain, anxiety, medication effect and hypoglycaemia.
Syncope with pelvic pain or bleeding is an ectopic-pregnancy emergency until proven otherwise.

E — Exposure

Inspect for pallor, fever, abdominal distension, bruising, scars, vaginal bleeding and signs of infection while protecting dignity.
Perform abdominal examination; pelvic/rectal examination requires consent, chaperone and appropriately trained staff.

Focused history

History area	Questions	Why it matters
Pain	Onset, site, severity, cyclical pattern, sudden vs gradual, radiation to shoulder/back, triggers and response to medicine.	Distinguishes chronic endometriosis from torsion, rupture, ectopic, appendicitis or renal colic.
Menstrual	Last period, cycle, flow, clots, intermenstrual bleeding and pain before/during/after menstruation.	Assesses disease pattern, anaemia and pregnancy risk.
Pregnancy/fertility	Sexual activity, contraception, pregnancy intention, infertility duration and previous ectopic/miscarriage.	Pregnancy test changes urgent differential and imaging/treatment choices.
Bowel/bladder	Painful stool/urination, diarrhoea, constipation, rectal/urinary blood, inability to pass urine/stool.	Identifies deep disease, obstruction, infection or bleeding.
Previous care	Ultrasound/MRI, surgery, endometrioma, hormonal medicines, analgesics and response/side effects.	Guides safe acute treatment and specialist referral.
Safety/mental health	Impact on school/work, sleep, relationships, mood, coercion or sexual violence.	Chronic pain is associated with distress and requires holistic support.

Differential diagnosis of acute pelvic pain

Condition	Clues	Immediate action
Ectopic pregnancy	Positive/uncertain pregnancy, unilateral pain, bleeding, syncope, shoulder pain or shock.	Pregnancy test, IV access, resuscitation and urgent gynaecology/surgery.
Ovarian torsion	Sudden unilateral severe pain, vomiting, adnexal mass or intermittent attacks.	Urgent ultrasound and gynaecology; ovarian salvage is time-sensitive.
Ruptured endometrioma/cyst	Sudden pain, peritoneal signs, anaemia or haemoperitoneum.	Analgesia, fluids, haemoglobin/crossmatch and urgent imaging/surgical review.
PID/tubo-ovarian abscess	Fever, discharge, pelvic tenderness, dyspareunia or sepsis.	Pregnancy test, cultures where indicated, antibiotics and admission if severe.
Appendicitis/obstruction	Right lower quadrant pain, guarding, vomiting, distension or altered bowel habit.	Surgical assessment, IV fluids, analgesia and imaging.
Renal/urinary causes	Flank pain, haematuria, dysuria, fever or urinary retention.	Urinalysis, renal function, analgesia and obstruction/infection pathway.

Investigations

Urine or serum pregnancy test in every patient of reproductive potential with pelvic pain or bleeding, regardless of stated contraception.
Full blood count for anaemia/infection, group and crossmatch when bleeding or surgery is possible, CRP, renal function, electrolytes and urinalysis.
STI testing/swabs when discharge, pelvic tenderness or risk factors are present; test and treat sensitively.
Pelvic ultrasound (transabdominal or transvaginal according to age, consent and local practice) to assess endometrioma, torsion, pregnancy and other pathology. NICE advises ultrasound even when examination is normal and does not recommend CA-125 as a diagnostic test.
MRI or laparoscopy may be used by specialist teams for deep disease or uncertain diagnosis; a normal scan does not exclude endometriosis.

Immediate management of severe pain without instability

Use a pain score and reassess after each intervention. Offer heat, positioning, privacy and calm explanation.
Give prescribed paracetamol/acetaminophen and/or an NSAID when not pregnant and no renal disease, ulcer, anticoagulation or allergy; follow local dose limits.
Use antiemetics for vomiting and short-course titrated opioid analgesia only when pain is severe and monitored care is available.
Do not delay pregnancy testing or urgent imaging because analgesia was given; adequate analgesia improves examination and does not “mask” a diagnosis when reassessment continues.
Refer for same-day gynaecology review when pain is uncontrolled, recurrent with functional impairment, associated with mass, infertility or abnormal bleeding.

Management of haemorrhage, shock or acute abdomen

Activate emergency and surgical/gynaecology response; keep the patient nil by mouth if operative intervention is possible.
Two IV lines where feasible, blood tests/crossmatch, isotonic crystalloid for shock, warming and repeated vital signs.
Manage ectopic pregnancy, torsion, ruptured cyst/endometrioma, perforation or obstruction according to the specialist pathway; do not send an unstable patient for outpatient follow-up.
Monitor haemoglobin, urine output, lactate, pain, abdominal signs and response to fluids; escalate persistent hypotension or peritonism.

Planned medical and hormonal treatment

Analgesic plans may include NSAIDs or paracetamol, with review of effectiveness, renal/GI risk and medication overuse.
Hormonal suppression (combined hormonal contraceptive, progestogen, levonorgestrel intrauterine system or specialist GnRH therapy) may reduce cyclical pain and bleeding; discuss contraindications, fertility goals and side effects.
Hormonal therapy controls symptoms but does not remove all lesions. Pain may recur after stopping treatment and requires follow-up.
Refer to a specialist endometriosis service for suspected deep disease, endometrioma, bowel/bladder/ureter involvement, persistent pain, infertility or failed first-line treatment.

Surgical and fertility considerations

Laparoscopic excision/ablation, adhesiolysis or endometrioma surgery may be considered after shared decision-making; ovarian surgery can affect reserve and should be planned carefully.
Discuss whether pregnancy is a current priority before hormonal suppression. Fertility referral may include expectant management, ovulation treatment or assisted reproduction depending on age, ovarian reserve and tubal/partner factors.
Hysterectomy is not a universal cure and is considered only for selected patients who have completed childbearing and understand persistent extra-uterine pain may remain.

Nursing and EMT interventions

Reassess pain, vital signs, bleeding, nausea, urine output and abdominal signs; document the patient’s words and functional impact.
Provide dignity, a chaperone and trauma-informed care; avoid judgement about sexual history, fertility, menstruation or pain behaviours.
Monitor NSAID, opioid and hormonal adverse effects; assess renal function, GI bleeding, constipation, sedation and pregnancy status.
Support hydration, nutrition, iron evaluation when heavy bleeding is present and safe mobilisation.
Use teach-back for warning signs: collapse, sudden one-sided pain, fever, vomiting, heavy bleeding, inability to pass urine/stool and positive pregnancy test.
Provide written follow-up and ensure referral is not lost when symptoms are chronic or imaging is normal.

Prevention and self-management support

Encourage a symptom/menstrual diary recording pain, bleeding, bowel/bladder symptoms, medicines, school/work impact and triggers.
Take prescribed medicines early in the pain cycle when advised; avoid exceeding dose limits or combining duplicate NSAIDs.
Use heat, sleep support, graded activity, pelvic-floor physiotherapy or psychological pain support when appropriate.
Seek care early for heavy bleeding or anaemia and maintain contraception/pregnancy planning discussions.
Remember that early recognition and respectful listening reduce diagnostic delay; there is no single blood test that excludes endometriosis.

Clinical scenarios

Scenario 1 — Sudden unilateral pain: A woman with known endometriosis develops abrupt right-sided pain, vomiting and faintness. Do not assume a routine flare. ABCDE, pregnancy test, IV access, analgesia, fluids if shocked and urgent ultrasound/gynaecology review for torsion, ectopic pregnancy or ruptured cyst.

Scenario 2 — Chronic severe dysmenorrhoea: A student misses class every month because of pain and diarrhoea. She is stable. Take a detailed menstrual/bowel history, validate the symptoms, rule out pregnancy/infection when indicated, offer safe analgesia and arrange ultrasound and gynaecology review rather than repeated emergency-only analgesia.

Scenario 3 — Deep disease: A patient has cyclical rectal bleeding, painful defecation and anaemia. Assess haemodynamic status, full blood count and stool/rectal symptoms, refer to a specialist endometriosis and colorectal pathway, and urgently investigate any heavy bleeding, obstruction or peritonism.

Common errors to avoid

Normalising severe period pain or calling it psychological without assessment.
Failing to perform a pregnancy test in pelvic pain or bleeding.
Attributing sudden pain to endometriosis and missing torsion, ectopic pregnancy, appendicitis, sepsis or obstruction.
Performing pelvic examination without consent, chaperone, explanation or trauma-informed care.
Using CA-125 or a normal ultrasound as a reason to dismiss symptoms.
Giving repeated analgesics without a plan for diagnosis, follow-up, fertility goals and functional impact.

PELVIC SAFE: P — Pregnancy test; E — Evaluate ABCDE and ectopic/torsion; L — Listen to pain history; V — Vital signs/bleeding; I — Investigate urine, blood and ultrasound; C — Consent/chaperone; S — Safe analgesia; A — Assess bowel/bladder; F — Fertility goals; E — Escalate red flags.

Revision questions

Define endometriosis and explain how lesions cause cyclical pain and adhesions.
List common bowel, bladder, reproductive and thoracic symptoms.
Why is a pregnancy test essential in acute pelvic pain?
Differentiate endometriosis flare, ovarian torsion, ruptured endometrioma and ectopic pregnancy.
What consent and privacy principles apply before pelvic examination?
Outline emergency care for the unstable patient in Scenario 1.

Key takeaways

Endometriosis pain is real, chronic and treatable—but acute pelvic pain still requires an emergency differential. Check pregnancy, assess haemorrhage and sepsis, rule out torsion/ectopic/obstruction, provide respectful analgesia and connect the patient to long-term gynaecology and fertility care.

References for further study

WHO. Endometriosis fact sheet, updated 2025.
NICE. Endometriosis: diagnosis and management (NG73), updated 2024.
Royal College of Obstetricians and Gynaecologists. Endometriosis patient information.
ACOG. Endometriosis and updated diagnosis guidance.
Follow current Uganda Ministry of Health and specialist gynaecology protocols for acute pelvic pain, pregnancy, analgesia and surgery.

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Adrenal Suppression and Adrenal Crisis: Emergency Recognition, Assessment and Management

Adrenal Suppression and Adrenal Crisis: Recognition, Assessment and Emergency Management

Why this topic matters: Long-term or high-dose glucocorticoids can suppress the hypothalamic–pituitary–adrenal (HPA) axis. The adrenal glands then cannot produce enough cortisol during infection, trauma, surgery, vomiting or other stress. Abruptly stopping steroids may cause life-threatening adrenal crisis with hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia, shock and coma. EMTs must identify steroid dependence, give emergency hydrocortisone under protocol without waiting for laboratory confirmation, restore circulation and communicate the last dose and trigger.

Learning objectives

Explain HPA-axis suppression, primary, secondary and tertiary adrenal insufficiency and the difference between withdrawal symptoms and adrenal crisis.
Recognise chronic symptoms, acute red flags and the common triggers of crisis.
Perform a rapid ABCDE assessment with glucose, electrolytes, ECG, shock and infection evaluation.
Describe emergency hydrocortisone, isotonic fluid, dextrose, electrolyte and precipitant management.
Teach steroid tapering, sick-day rules, emergency cards, injection skills and safe follow-up.

Cortisol and the HPA axis

Stress activates the hypothalamus to release corticotropin-releasing hormone (CRH), which stimulates pituitary ACTH. ACTH stimulates the adrenal cortex to produce cortisol. Cortisol maintains vascular responsiveness to catecholamines, supports glucose production, controls inflammation and helps the body tolerate infection, surgery and trauma. Cortisol secretion normally rises sharply during serious illness.

Exogenous glucocorticoids provide negative feedback, reducing CRH and ACTH. After prolonged suppression, the adrenal cortex becomes less responsive and may need weeks to months to recover. The 2024 ESE/Endocrine Society guideline considers oral exposure a risk when treatment lasts about 3–4 weeks or longer and the dose exceeds approximately 15–25 mg hydrocortisone equivalent daily (for example, 4–6 mg prednisone/prednisolone), although risk varies with route, timing, potency and individual susceptibility.

Types of adrenal insufficiency

Type	Mechanism and causes	Typical clues
Primary	Adrenal gland damage: autoimmune Addison disease, tuberculosis, HIV, haemorrhage, metastasis, bilateral adrenalectomy or certain medicines.	Low cortisol and aldosterone, hyponatraemia, hyperkalaemia, dehydration, postural hypotension and hyperpigmentation.
Secondary	Low ACTH from pituitary disease, surgery, irradiation, traumatic brain injury or infiltrative disease.	Low cortisol; aldosterone is usually preserved, so potassium may remain normal and hyperpigmentation is absent.
Tertiary / glucocorticoid-induced	Suppressed CRH/ACTH after long-term steroids or after successful treatment of Cushing syndrome.	Recent taper/cessation, fatigue, nausea, weakness, low BP, hypoglycaemia during illness and poor stress tolerance.

Causes and risk settings

Oral prednisolone, prednisone, dexamethasone or hydrocortisone for inflammatory disease, asthma, autoimmune disease, cancer or transplant care.
Repeated intra-articular/epidural injections, potent topical steroids, high-dose inhaled steroids or steroid-containing traditional/beauty products.
Recent rapid taper, missed doses, abrupt discontinuation, vomiting, malabsorption or inability to obtain medication.
Critical illness: fever, sepsis, malaria, gastroenteritis, trauma, surgery, burns, childbirth, severe pain or prolonged fasting.
Medicines that alter steroid metabolism, pituitary disease, adrenal haemorrhage, bilateral adrenalectomy or treatment of Cushing syndrome.

Chronic symptoms before crisis

Persistent fatigue, weakness, reduced exercise tolerance, dizziness, weight loss, poor appetite, nausea or abdominal discomfort.
Low blood pressure, postural symptoms, salt craving, dehydration, muscle/joint aches and recurrent unexplained hypoglycaemia.
Hyponatraemia, hyperkalaemia, eosinophilia, anaemia or low glucose on previous laboratory tests.
Hyperpigmentation of skin creases, scars, palmar lines or oral mucosa suggests primary disease; it may be absent in secondary/tertiary suppression.
Glucocorticoid withdrawal syndrome can cause myalgia, arthralgia, lethargy, mood change and nausea even without dangerous cortisol deficiency; crisis must still be excluded during acute illness.

Adrenal crisis red flags: sudden severe weakness, vomiting/diarrhoea, abdominal or back pain, confusion, collapse, profound hypotension, shock, hypoglycaemia, hyponatraemia, hyperkalaemia, fever/hypothermia or deterioration after missed/stopped steroids.

First contact and scene priorities

Use standard precautions and look for steroid packets, emergency cards, injection kits, medical-alert jewellery and recent discharge letters.
Call for emergency transport and senior support. Adrenal crisis is a medical emergency even if the patient has no confirmed diagnosis.
Ask the patient or relative: steroid name, route, dose, last dose, duration, recent taper, vomiting, illness, surgery, pregnancy and access barriers.
Position for shock while protecting the airway; use a lateral position if vomiting or reduced consciousness and no contraindication.
Do not delay emergency hydrocortisone for cortisol/ACTH results. If blood can be collected without delaying treatment, take it first.

ABCDE assessment

A — Airway

Assess speech, secretions, vomiting and consciousness; hypoglycaemia, shock and electrolyte disturbance may impair airway protection.
Suction and provide airway support as trained. Prepare for advanced management when GCS is falling.

B — Breathing

Count respiratory rate, measure SpO₂ and look for sepsis, aspiration, pulmonary oedema and metabolic acidosis.
Give oxygen for hypoxaemia or respiratory distress according to local protocol; do not mistake compensatory tachypnoea for a primary lung disease without assessment.

C — Circulation

Check pulse, BP (including postural change when safe), capillary refill, temperature, peripheral perfusion and urine output.
Establish IV/IO access in shock; obtain electrolytes, glucose, cortisol/ACTH, urea/creatinine, blood count, blood gas and cultures when feasible.
Start isotonic saline rapidly for hypotension under the adrenal-crisis protocol and reassess lungs, perfusion and urine output.

D — Disability

Record AVPU/GCS, pupils, confusion and seizures. Check bedside glucose immediately and repeat after dextrose.
Severe hyponatraemia can cause headache, confusion and seizures; hyperkalaemia can cause weakness and fatal dysrhythmia.

E — Exposure

Measure temperature, inspect for infection, wounds, hyperpigmentation, dehydration, abdominal tenderness, trauma and steroid injection sites.
Preserve warmth and dignity; avoid unnecessary exposure in a shocked patient.

Focused history

History area	Questions	Clinical value
Glucocorticoid exposure	Which medicine, dose, route, duration, last dose, recent taper, injection/inhaler/cream or traditional product?	Estimates suppression risk and replacement needs.
Illness/stress	Fever, infection, vomiting, diarrhoea, injury, surgery, burns, labour, fasting or severe pain?	Identifies increased cortisol demand and the crisis trigger.
Symptoms	Weakness, dizziness, salt craving, abdominal pain, weight loss, confusion, fainting or palpitations?	Supports adrenal insufficiency and complication recognition.
Medicines	Diabetes drugs, diuretics, anticoagulants, opioids, antifungals, enzyme inducers and antihypertensives?	Explains glucose/electrolyte changes and interactions.
Support/safety	Emergency card, injection training, family support, medicine supply, health literacy and previous crisis?	Guides discharge prevention and immediate assistance.

Investigations

Bedside glucose and repeat measurements; obtain venous/arterial blood gas and lactate in shock or severe illness.
Serum sodium, potassium, bicarbonate, urea/creatinine, calcium, magnesium, full blood count and ECG for dysrhythmia/hyperkalaemia.
Take serum cortisol and ACTH before hydrocortisone only if this causes no delay; a random cortisol may be difficult to interpret after exogenous steroid exposure.
After stabilisation, endocrine testing may include morning cortisol, ACTH stimulation test, renin/aldosterone, antibodies and pituitary/adrenal imaging to determine the cause.
Search for triggers with cultures, urinalysis, malaria testing where relevant, chest imaging, pregnancy testing and targeted tests for trauma, MI, PE or abdominal disease.

Immediate treatment of suspected adrenal crisis

Hydrocortisone: give 100 mg IV or IM immediately in adults under the emergency protocol. Do not wait for laboratory confirmation.
Fluids: rapidly rehydrate with 0.9% saline or an approved isotonic crystalloid, reassessing BP, lungs, urine output, sodium and heart/renal status.
Glucose: treat documented hypoglycaemia with IV dextrose or oral carbohydrate only when swallowing is safe; add dextrose to IV fluid when clinically indicated.
Continuation: hospital protocols commonly use hydrocortisone 200 mg over 24 hours by continuous infusion or 50 mg IV/IM every 6 hours after the initial dose.
Trigger: treat sepsis, gastroenteritis, trauma, bleeding, surgery, malaria, MI or other precipitant using the appropriate pathway.
Electrolytes: monitor and manage hyperkalaemia, hyponatraemia, acidosis and renal impairment with senior/critical-care support.

Safety boundary: Exact fluid volumes, hydrocortisone regimen, paediatric doses and potassium treatment must follow the current Uganda facility protocol. In a suspected crisis, emergency hydrocortisone is safer than waiting for a cortisol result.

Hospital management and transition

Admit to a monitored area until BP, electrolytes, glucose, mental state and the precipitating illness are stable.
Continue parenteral hydrocortisone while vomiting, hypotension or severe illness persists; switch to oral replacement only when the patient is stable and absorbing reliably.
Adjust fluids for heart failure, kidney failure, older age and ongoing losses. Monitor for pulmonary oedema and rapid sodium correction.
Consult endocrinology to establish whether suppression is primary, secondary or tertiary and to plan tapering, replacement and testing of recovery.
Never stop the only source of glucocorticoid abruptly. Taper only when the underlying disease is controlled and the prescriber/endocrine team directs it.

Tapering and assessing recovery

Step	Principle	What the EMT/nurse should reinforce
Review indication	Taper only when the disease requiring steroid therapy is controlled and steroids are no longer essential.	Do not reduce doses independently because symptoms improve.
Approach physiologic dose	Reduce gradually toward a physiologic equivalent, often around 4–6 mg prednisone/prednisolone daily, under specialist advice.	Report weakness, dizziness, nausea, hypotension and hypoglycaemia during taper.
Assess axis recovery	Morning cortisol and/or ACTH stimulation testing may be used when clinically appropriate.	Recovery is variable; continue precautions until confirmed.
Stress cover	Increase glucocorticoid during significant illness, surgery, trauma or labour according to written plan.	Carry emergency information and know when to inject/call for help.

Nursing and EMT care

Trend BP, pulse, mental state, temperature, capillary glucose, sodium, potassium, fluid balance and urine output.
Check IV/IM hydrocortisone dose, time, route and response; use an independent check where policy requires.
Maintain aspiration, falls and seizure precautions; provide oral care and safe repositioning.
Inspect IV sites, monitor fluid response and report crackles, increasing oxygen need, oedema or absent urine.
Use SBAR to hand over last steroid dose, time of hydrocortisone, glucose/potassium values, suspected trigger and response to fluids.
Teach the patient and family with teach-back: daily replacement, sick-day rules, injection practice, card/bracelet and emergency contact.

Prevention and steroid safety

Carry a steroid emergency card or medical-alert identification and keep an emergency hydrocortisone injection available when prescribed.
Never stop long-term steroids suddenly, miss doses during illness or assume inhaled/topical/injected steroids are risk-free.
During vomiting, diarrhoea or severe illness, follow the written sick-day plan and seek help if oral medication cannot be absorbed.
Tell every clinician, dentist, midwife and emergency responder about steroid dependence before procedures or surgery.
Keep a reserve supply, check expiry and storage, and ensure family/co-workers know when and how to give emergency injection.
Review bone health, infection prevention, blood pressure, glucose and eye care during long-term glucocorticoid treatment.

Clinical scenarios

Scenario 1 — Vomiting after taper: A woman who completed a rapid prednisolone taper develops vomiting, severe weakness, BP 75/45 and glucose 2.8 mmol/L. Suspect adrenal crisis: ABCDE, IV/IO access, immediate hydrocortisone, isotonic saline, dextrose for hypoglycaemia, ECG/electrolytes and urgent transfer. Do not wait for a cortisol result.

Scenario 2 — Steroid card prevents delay: A man with known adrenal insufficiency collapses with gastroenteritis. His family shows the emergency card and injection kit. Give the prescribed emergency hydrocortisone promptly, monitor airway/circulation, start fluids under protocol and communicate the kit dose/time to the receiving team.

Scenario 3 — Chronic inhaled and topical exposure: A patient says they take no “tablets” but uses high-dose inhaled steroid, potent skin cream and repeated joint injections. They are weak and hypotensive during pneumonia. Ask about all routes, suspect suppression, treat the acute illness and escalate for emergency steroid cover.

Common errors to avoid

Waiting for cortisol/ACTH results before giving hydrocortisone in suspected crisis.
Stopping chronic steroids abruptly or failing to stress-dose during major illness, surgery, trauma or labour.
Missing adrenal suppression because the steroid is inhaled, topical, injected or obtained outside the formal prescription list.
Treating hypotension with fluids alone while ignoring cortisol deficiency, hypoglycaemia, hyperkalaemia or sepsis.
Giving large fluid volumes without reassessing lungs, renal function, sodium and urine output.
Discharging without an emergency card, injection plan, supply check and clear follow-up.

STEROID CRISIS: S — Search for steroid exposure; T — Treat ABCDE; E — Emergency hydrocortisone; R — Rehydrate with isotonic fluid; O — Observe glucose/electrolytes; I — Identify infection/trigger; D — Dextrose if hypoglycaemic; C — Cardiac/ECG monitoring; R — Repeat vitals and urine; I — Inform endocrine team; S — Sick-day education; I — Identification card/injection; S — Safe taper; E — Escalate deterioration.

Revision questions

Explain how long-term glucocorticoids suppress the HPA axis.
What treatment exposure and duration commonly place an adult at risk of adrenal suppression?
List six symptoms/signs of adrenal crisis and four common precipitants.
Why should hydrocortisone not be delayed for cortisol or ACTH results?
Describe the emergency sequence for a patient with shock and hypoglycaemia after steroid withdrawal.
What education and equipment should a steroid-dependent patient have before discharge?

Key takeaways

Adrenal crisis is a preventable shock state. Ask about every steroid route, recognise hypotension plus weakness/vomiting/hypoglycaemia, give emergency hydrocortisone promptly, restore circulation, treat the trigger and ensure lifelong safety planning until recovery is proven.

References for further study

European Society of Endocrinology/Endocrine Society. Glucocorticoid-Induced Adrenal Insufficiency Guideline, 2024.
Society for Endocrinology. Adrenal Crisis Information — immediate hydrocortisone and fluid guidance.
NICE. Adrenal insufficiency: identification and management, 2024.
NIDDK. Treatment for Adrenal Insufficiency and Addison’s Disease.
Follow current Uganda Ministry of Health, hospital and endocrine protocols for adult, paediatric, pregnancy and perioperative stress-dose care.

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Thyroid Storm: Emergency Recognition, Assessment and Management

Why this topic matters: Thyroid storm is acute, life-threatening decompensation from severe thyrotoxicosis. It can cause extreme tachycardia, hyperthermia, agitation or coma, vomiting/diarrhoea, heart failure, atrial fibrillation, shock, liver injury and death. It is often precipitated by infection, trauma, surgery, labour, iodine exposure, diabetic ketoacidosis or stopping antithyroid treatment. Diagnosis is clinical; do not wait for thyroid results before resuscitation and specialist treatment.

Learning objectives

Define thyroid storm and explain how excess thyroid hormone produces multi-organ decompensation.
Recognise the clinical spectrum from untreated hyperthyroidism to storm, including atypical and apathetic presentations.
Perform a rapid ABCDE assessment, severity score, focused history and precipitant search.
Describe hospital treatment sequence: supportive care, beta-blockade, thionamide, iodine, glucocorticoid and cause control.
Plan nursing monitoring, complication prevention, discharge education and special-population care.

Definition and pathophysiology

The thyroid produces thyroxine (T4) and triiodothyronine (T3), hormones that increase oxygen consumption, heat production, cardiac contractility, heart rate and sensitivity to catecholamines. Thyroid storm is not defined by a single hormone level; it is a clinical syndrome in which thyrotoxicosis is accompanied by fever and central nervous, cardiovascular, gastrointestinal/hepatic or other organ dysfunction.

Excess thyroid hormone accelerates metabolism and increases beta-adrenergic activity. A trigger such as infection or surgery increases catecholamines, cortisol demand and inflammatory stress. The result may be hyperthermia, dehydration, high-output heart failure progressing to cardiogenic shock, atrial fibrillation, delirium, hepatic dysfunction, lactic acidosis and multi-organ failure.

Causes and precipitating events

Cause/trigger	Examples	Clues to search for
Underlying thyrotoxicosis	Graves disease, toxic multinodular goitre, toxic adenoma or thyroiditis.	Goitre, ophthalmopathy, tremor, weight loss, heat intolerance, palpitations.
Infection	Pneumonia, urinary infection, gastroenteritis, wound infection, malaria or sepsis.	Fever may be absent in older/immunosuppressed patients; look for subtle sources.
Medicine interruption	Stopped carbimazole/methimazole/PTU, poor access, vomiting or incorrect dose.	Medication history, empty packets and recent clinic interruption.
Physiological stress	Surgery, trauma, labour, myocardial infarction, stroke, DKA or pulmonary embolism.	Recent operation, delivery, chest pain, focal deficit, hyperglycaemia or hypoxia.
Iodine/drug exposure	Contrast, amiodarone, excess iodine, some biologic medicines.	Recent imaging, antiarrhythmic use or new specialist medication.

Clinical features

Thermoregulatory: high fever, hot sweaty skin, flushing, dehydration and heat intolerance.
Cardiovascular: marked tachycardia, wide pulse pressure, atrial fibrillation, chest pain, high-output failure, pulmonary oedema, hypotension or shock.
Neurological/psychiatric: anxiety, agitation, delirium, psychosis, confusion, lethargy, seizure or coma. Older adults may present with apathetic storm and little fever.
Gastrointestinal/hepatic: nausea, vomiting, diarrhoea, abdominal pain, jaundice and acute liver dysfunction.
Thyroid signs: goitre, bruit, tremor, hyperreflexia, lid retraction, ophthalmopathy and proximal weakness.
Metabolic: hyperglycaemia, lactic acidosis, dehydration and electrolyte abnormalities.

Emergency red flags: temperature ≥38–39°C with altered mental state, heart rate ≥140/min, atrial fibrillation, pulmonary oedema, chest pain, hypotension, severe vomiting/diarrhoea, jaundice, seizure, coma or rapidly worsening weakness. Call for senior/critical-care help and transfer urgently.

First contact and scene management

Use standard precautions; check the scene for collapse, vomit, medication containers and heat exposure.
Activate emergency transport and senior clinical support. A suspected storm requires hospital-level monitoring, IV medicines and treatment of the precipitant.
Move the patient to a cool, well-ventilated area, remove excess clothing and begin gentle cooling. Avoid shivering, ice immersion or vigorous rubbing.
Ask relatives to bring antithyroid medicines, beta-blocker, recent results, diabetes medicines and details of infection, surgery, pregnancy or iodine exposure.
Do not delay ABCDE, glucose and ECG for thyroid tests; do not give aspirin/salicylates to reduce fever because they may increase free thyroid hormone.

ABCDE assessment

A — Airway

Assess speech, secretions, vomiting, agitation and consciousness. Delirium, fatigue or coma may compromise airway protection.
Prepare suction and advanced airway support if the patient cannot protect the airway; involve anaesthesia/critical care early.

B — Breathing

Count respiratory rate, assess effort and measure SpO₂. Look for pulmonary oedema, aspiration, pneumonia and metabolic acidosis.
Give oxygen for hypoxaemia or respiratory distress according to local protocol; use non-invasive/invasive support with expert help if necessary.

C — Circulation

Monitor pulse, BP, ECG, capillary refill, temperature, peripheral perfusion and urine output continuously in severe illness.
Identify atrial fibrillation, narrow-complex tachycardia, ischaemia, high-output failure or shock. Obtain IV access and bloods.
Give cautious isotonic fluid for dehydration, balancing pulmonary oedema and heart failure risk. If shock persists, involve critical care for vasoactive support.

D — Disability

Record AVPU/GCS, pupils, agitation, delirium and seizure activity. Check bedside glucose to exclude hypoglycaemia or identify stress hyperglycaemia/DKA.
Screen for stroke, intoxication, meningitis, heat stroke and other causes of altered consciousness.

E — Exposure

Measure core temperature, inspect for goitre, ophthalmopathy, infection, surgical wounds and trauma.
Maintain dignity while removing excess clothing, applying cooling measures and searching for infection or thromboembolism.

Focused history and examination

Question/exam	What to establish	Why it matters
Thyroid history	Graves, goitre, thyroiditis, radioiodine, surgery, previous storm or recent abnormal results.	Identifies baseline risk and likely cause.
Medication adherence	Last carbimazole/methimazole/PTU, beta-blocker, amiodarone, steroids and missed doses.	Interruption is a common precipitant; amiodarone may cause thyroid dysfunction.
Trigger screen	Fever, cough, dysuria, diarrhoea, wounds, chest pain, trauma, surgery, labour, contrast, DKA or stroke symptoms.	Treating the precipitant is as important as controlling hormone effects.
Heart/lung exam	Pulse rhythm, JVP, crackles, oedema, murmurs, chest pain and signs of PE.	Guides cautious beta-blockade, fluids, diuresis and critical-care escalation.
Neuro/eye/neck	Agitation, delirium, tremor, hyperreflexia, goitre bruit, eye pain/visual change.	Assesses severity and identifies thyroid eye or pituitary/neurological differentials.

Severity scoring and diagnosis

The Burch–Wartofsky Point Scale considers temperature, tachycardia, gastrointestinal/hepatic dysfunction, central nervous system effects, heart failure and a precipitating event. A high score supports storm but does not replace clinical judgement.
Japanese Thyroid Association criteria emphasise thyrotoxicosis plus fever, tachycardia, heart failure, gastrointestinal/hepatic symptoms and CNS disturbance.
Thyroid storm is a clinical diagnosis. TSH is usually suppressed and free T4/free T3 elevated, but hormone levels overlap with uncomplicated thyrotoxicosis and results may be delayed.
Do not withhold treatment while waiting for TSH, free T4 or free T3 when the patient has organ dysfunction and a compatible history.

Investigations

Bedside glucose, continuous ECG, full blood count, electrolytes, urea/creatinine, magnesium, liver tests, CRP/lactate and venous/arterial blood gas when critically ill.
TSH, free T4, free T3, thyroid antibodies when helpful; cortisol may be taken before steroids if this does not delay treatment.
Blood/urine cultures, malaria testing where relevant, urinalysis, chest imaging, ECG/troponin, echocardiography and pregnancy test as indicated.
Consider CT pulmonary angiography, brain imaging or abdominal imaging for pulmonary embolism, stroke, trauma, severe abdominal pain or liver pathology.

Immediate supportive treatment

Admit to a monitored resuscitation, high-dependency or intensive-care environment according to severity.
Control temperature with cooling blankets, tepid sponging, fans and paracetamol/acetaminophen if liver function and local protocol allow. Avoid salicylates.
Correct dehydration carefully with isotonic crystalloid; treat hypoglycaemia, electrolyte disturbance and hypoxia promptly.
Manage agitation safely with a calm low-stimulation environment and carefully titrated medication prescribed by the senior team; avoid excessive sedation that masks neurological deterioration.
Start empiric antimicrobials promptly when infection is suspected after cultures where feasible; do not wait for thyroid results.

Specific hospital treatment sequence

Order	Therapy	Purpose and cautions
1. Beta-blockade	Propranolol or short-acting esmolol under specialist monitoring; diltiazem may be considered when beta-blockade is unsafe.	Controls adrenergic symptoms and tachycardia. Use extreme caution in shock, decompensated heart failure, severe asthma or cardiogenic pulmonary oedema.
2. Thionamide	PTU or methimazole/carbimazole by oral, nasogastric or specialist-approved route.	Blocks new hormone synthesis; PTU also reduces T4-to-T3 conversion. Check liver injury/agranulocytosis risk and follow local dosing.
3. Iodine	Potassium iodide/Lugol’s iodine after the thionamide, usually separated by at least one hour.	Blocks hormone release. Giving iodine before thionamide can provide substrate for new hormone synthesis.
4. Glucocorticoid	Hydrocortisone or dexamethasone IV under the emergency protocol.	Supports possible relative adrenal insufficiency and reduces T4-to-T3 conversion; monitor glucose, infection and psychiatric effects.
5. Treat the trigger	Antibiotics/source control, ACS/PE/stroke pathways, trauma care, DKA management or obstetric support.	Storm will not resolve if the precipitant is missed.

Sequence matters: In hospital, thionamide is generally given before iodine. Exact drug, route and dose depend on age, pregnancy, liver function, heart failure, asthma and local protocol. EMTs should not independently initiate specialist antithyroid regimens without an authorised protocol and monitoring.

Cardiovascular and rhythm management

Continuous ECG and frequent BP assessment are essential. Treat hypoxia, fever, dehydration and electrolyte abnormalities that worsen tachycardia.
Atrial fibrillation may require rate control, anticoagulation assessment and cardiology input. Avoid reflexively giving a beta-blocker to a patient in shock or acute decompensated heart failure.
Use diuretics for pulmonary oedema when prescribed; consider echocardiography, inotropes or vasopressors in cardiogenic shock with critical-care support.
Cardioversion is reserved for selected unstable rhythms after senior review because recurrence is common while thyrotoxicosis persists.

Monitoring and nursing care

Trend temperature, heart rate/rhythm, BP, respiratory rate, SpO₂, GCS/mental state, urine output and fluid balance closely.
Repeat glucose, electrolytes, magnesium, liver function, lactate and blood gases according to severity and treatment.
Maintain cooling, skin care, pressure-area care and safe hydration; avoid shivering and monitor for cold injury.
Use fall, seizure, aspiration and delirium precautions. Keep the environment quiet and explain procedures repeatedly.
Check every drug, timing and route; document antithyroid, beta-blocker, iodine and steroid administration and the response.
Watch for thionamide adverse effects: rash, fever, sore throat/agranulocytosis, hepatitis and pancreatitis. Report new fever or throat pain urgently.
Communicate trends during SBAR handover, including suspected trigger, highest temperature, heart rhythm, GCS, fluid balance and treatments.

Complications

High-output heart failure progressing to pulmonary oedema, cardiogenic shock or cardiac arrest.
Atrial fibrillation, ventricular dysrhythmia, myocardial ischaemia and thromboembolism.
Hyperthermia, dehydration, acute kidney injury, lactic acidosis and electrolyte disturbance.
Delirium, seizure, coma, aspiration and traumatic injury.
Acute liver failure, jaundice, coagulopathy and hypoglycaemia.
Medication harm: bronchospasm or shock from beta-blockade, liver toxicity from PTU, agranulocytosis from thionamides and hyperglycaemia/infection from steroids.

Special populations

Pregnancy/labour: involve obstetrics and endocrinology; fetal tachycardia and maternal heart failure may occur. Radioiodine is contraindicated; drug choice and dose are specialist decisions.
Heart failure/asthma: beta-blockers can cause collapse or bronchospasm; use a short-acting agent or alternative only with senior monitoring.
Liver disease: PTU may worsen hepatic injury; monitor liver tests and obtain specialist advice.
Older/apathetic patient: may have little fever or agitation but present with heart failure, delirium, weakness or collapse.
Children: use paediatric weight-based protocols and specialist input; do not apply adult doses.

Clinical scenarios

Scenario 1 — Infection-triggered storm: A woman with Graves disease stopped carbimazole and now has fever 40°C, HR 155, agitation, vomiting and crackles. Start ABCDE, oxygen for hypoxaemia, ECG/IV access, cautious fluid assessment, cooling and urgent transfer. Prepare for infection treatment, beta-blockade only after senior review, thionamide, iodine after thionamide and hydrocortisone.

Scenario 2 — Storm with heart failure: An older man has tachyarrhythmia, pulmonary oedema and confusion but only a low-grade fever. Suspect apathetic storm. Sit upright, oxygen/ventilatory support, ECG, cautious fluids, urgent cardiology/ICU help and avoid a large beta-blocker bolus that could cause cardiovascular collapse.

Scenario 3 — Iodine exposure: A patient with untreated goitre deteriorates after contrast imaging with tremor, fever and rapid atrial fibrillation. Treat the clinical syndrome immediately, monitor rhythm and heart failure, investigate infection/ACS/PE and alert the endocrine team about recent iodine exposure.

Common errors to avoid

Waiting for TSH, T3 or T4 results before treating a clinically unstable patient.
Giving aspirin/salicylates for fever, or giving iodine before thionamide without a specialist reason.
Using a large non-titrated beta-blocker dose in shock, severe asthma or decompensated heart failure.
Missing infection, myocardial infarction, DKA, pulmonary embolism, stroke, labour or medicine interruption as the trigger.
Assuming a quiet older patient cannot have storm because fever and agitation are absent.

STORM CARE: S — Support ABCDE and cooling; T — Tachycardia/temperature/trigger; O — Oxygen, glucose and ECG; R — Replace fluids cautiously; M — Medications in sequence; C — Control infection and complications; A — Avoid salicylates and unsafe beta-blockade; R — Reassess rhythm, GCS, urine and labs; E — Endocrine/critical-care escalation.

Revision questions

How does thyroid hormone excess produce tachycardia, hyperthermia and heart failure?
List six common precipitants of thyroid storm.
Why is thyroid storm a clinical diagnosis rather than a laboratory number?
State the usual sequence of beta-blocker, thionamide, iodine and glucocorticoid treatment.
When can beta-blockade be dangerous, and what monitoring is required?
Why should aspirin/salicylates be avoided for storm-related fever?
Write an SBAR handover for Scenario 1.

Key takeaways

Thyroid storm is a clinical, multi-organ emergency. Resuscitate first, cool safely, monitor the heart, check glucose/electrolytes, find and treat the precipitant, and coordinate specialist treatment in the correct sequence without waiting for thyroid results.

References for further study

Merck Manual Professional. Hyperthyroidism and Treatment of Thyroid Storm.
NHS. Overactive thyroid: complications — emergency signs of thyroid storm.
Society for Endocrinology. Clinical guidance and endocrine emergency resources.
American Thyroid Association. Professional thyroid disease resources.
Use current Uganda Ministry of Health, hospital, endocrine, cardiology and obstetric protocols for drug choice and dosing.

Thyroid Storm: Emergency Recognition, Assessment and Management Read More »

Cushing Syndrome: Recognition, Assessment and Emergency Management

Why this topic matters: Cushing syndrome is prolonged exposure to excessive cortisol, from prescribed glucocorticoids or abnormal endogenous cortisol production. Although the classic changes develop gradually, the patient may present to emergency care with severe hypertension, hyperglycaemia, hypokalaemia, infection, thromboembolism, psychosis, fracture, gastrointestinal bleeding or acute illness after steroid withdrawal. Emergency providers must recognise the phenotype, protect the patient from immediate complications, identify steroid exposure and coordinate urgent endocrine, medical and surgical care without abruptly stopping essential glucocorticoids.

Learning objectives

Define Cushing syndrome and distinguish exogenous steroid excess from endogenous ACTH/cortisol overproduction.
Recognise characteristic appearance, metabolic complications and red flags requiring emergency escalation.
Perform a structured ABCDE assessment and take a medication, infection, thrombotic and psychiatric history.
Describe appropriate investigations, acute stabilisation, complication management and definitive specialist treatment.
Explain why glucocorticoids must never be stopped abruptly and how to prevent steroid-related harm.

Definition and cortisol physiology

Cortisol is produced by the adrenal cortex under hypothalamic CRH and pituitary ACTH control. It supports vascular tone, glucose availability, stress responses, immune regulation and metabolism. Cushing syndrome is the clinical state caused by chronic exposure to cortisol or a glucocorticoid medicine above the body’s normal requirement. Cushing disease is the specific form caused by an ACTH-producing pituitary adenoma.

Excess cortisol increases gluconeogenesis and insulin resistance, promotes protein breakdown and skin thinning, redistributes fat, increases vascular sensitivity to catecholamines, suppresses immune responses and causes bone loss. Mineralocorticoid effects at high cortisol levels can produce sodium retention, hypertension and potassium loss. Exogenous steroids also suppress ACTH; sudden cessation can therefore precipitate adrenal insufficiency or crisis.

Causes and classification

Category	Examples	Emergency clues
Exogenous / iatrogenic	Long-term oral prednisolone, dexamethasone, hydrocortisone, repeated injections, potent inhaled/topical steroids or interacting medicines that increase steroid levels.	Medication list, proximal weakness, bruising, diabetes, infection, poor wound healing; risk of adrenal suppression if stopped suddenly.
ACTH-dependent endogenous	Pituitary corticotroph adenoma (Cushing disease) or ectopic ACTH/CRH from a tumour.	Rapid progression, severe hypokalaemia, muscle weakness, weight loss or malignancy symptoms suggest ectopic production.
ACTH-independent endogenous	Adrenal adenoma, carcinoma or bilateral adrenal hyperplasia.	Marked virilisation, abdominal mass, severe cortisol excess or rapidly progressive features need urgent specialist review.
Non-Cushing mimics	Alcohol excess, severe depression, obesity, poorly controlled diabetes, pregnancy and some medicines.	Confirm biochemically; do not label on appearance alone.

Typical clinical features

Weight gain with central/truncal obesity, rounded “moon” face, dorsocervical fat pad and relatively thin limbs.
Wide violaceous abdominal, breast or thigh striae; thin fragile skin, easy bruising, acne, facial plethora and slow wound healing.
Proximal muscle weakness, difficulty climbing stairs or rising from a chair, fatigue and osteoporosis with vertebral or rib fractures.
Hypertension, oedema, glucose intolerance/diabetes, dyslipidaemia and hypokalaemic metabolic alkalosis in severe cases.
Menstrual irregularity, reduced libido, infertility, hirsutism or virilisation; impaired growth in children.
Depression, anxiety, irritability, insomnia, impaired concentration, mania, psychosis or suicidal thoughts.
Frequent or atypical infection, oral thrush, urinary infection, pneumonia and poor response to vaccines.

Emergency red flags

Escalate immediately for: severe headache or visual loss, hypertensive emergency, chest pain or pulmonary embolism symptoms, sepsis, rapidly worsening weakness, hypokalaemic dysrhythmia, severe hyperglycaemia/DKA, acute psychosis or suicidality, gastrointestinal bleeding, new fracture, spinal cord compression or suspected adrenal crisis after steroid reduction.

Hypertensive emergency: very high BP with encephalopathy, seizures, chest pain, pulmonary oedema, renal injury or visual symptoms.
Thromboembolism: sudden dyspnoea, pleuritic pain, haemoptysis, unilateral leg swelling or unexplained tachycardia.
Severe infection: fever or hypothermia, confusion, hypotension, tachypnoea, new cough, dysuria or a subtle wound in an immunosuppressed patient.
Electrolyte crisis: weakness, cramps, palpitations, syncope or ECG changes suggesting hypokalaemia.

First contact and scene priorities

Use standard precautions and assess infection, fall, fracture, medication and self-harm risks.
Introduce yourself, obtain consent where possible and ask for all steroid containers, inhalers, creams, injections, diabetes medicines and recent hospital letters.
Assess airway, breathing and circulation before focusing on appearance. A patient who looks “Cushingoid” may still have sepsis, pulmonary embolism, stroke or myocardial infarction.
Do not abruptly discontinue prescribed glucocorticoids. Record the last dose and contact the prescriber/endocrine team urgently when the patient is acutely ill.
Use safe movement and fracture precautions; fragile bones, proximal weakness and obesity increase transfer and fall risk.

ABCDE assessment

A — Airway

Assess speech, secretions, facial infection, obesity-related obstruction, vomiting and reduced consciousness.
Consider aspiration, sepsis, sedative use or severe metabolic disturbance if mental status is abnormal.

B — Breathing

Count respiratory rate, measure SpO₂ and inspect for pneumonia, pulmonary oedema or pulmonary embolism.
Sudden breathlessness, pleuritic pain, haemoptysis or unexplained tachycardia is an emergency; give oxygen for hypoxaemia and arrange urgent transfer.

C — Circulation

Measure BP in both arms when indicated, pulse, capillary refill, temperature, peripheral oedema and urine output.
Check for shock, severe hypertension, dehydration, chest pain, irregular pulse and unilateral leg swelling.
Establish IV access in severe illness and collect glucose, electrolytes, renal function, full blood count and cultures when indicated.

D — Disability

Record AVPU/GCS, pupils, headache, visual fields, focal deficits, behaviour and suicide risk.
Check bedside glucose; cortisol excess can worsen diabetes, while steroid withdrawal can cause hypoglycaemia.

E — Exposure

Inspect skin, bruises, striae, wounds, injection sites, oral thrush, pressure areas, swelling and signs of fracture.
Measure temperature, weight if safe and signs of infection; preserve dignity and prevent heat loss.

Focused history

History	Questions	Why it matters
Steroid exposure	Which steroid, dose, route, duration, last dose, recent taper, injections, creams, inhalers or traditional medicines?	Identifies exogenous Cushing and risk of adrenal suppression.
Endocrine symptoms	Weight change, weakness, bruising, striae, menstrual change, libido, headache or visual problems?	Distinguishes chronic cortisol excess and pituitary mass effects.
Acute danger	Fever, cough, dysuria, wounds, chest pain, dyspnoea, leg swelling, severe headache, confusion or fracture?	Searches for infection, thromboembolism, stroke, fracture and hypertensive complications.
Metabolic history	Diabetes readings, thirst/urination, hypertension, potassium problems, kidney disease or heart failure?	Guides glucose, fluid and electrolyte risk.
Psychosocial	Sleep, mood, mania, hallucinations, suicidal thoughts, food access and support at home?	Cortisol excess can cause severe psychiatric illness and poor adherence.

Investigations

Immediate tests: bedside glucose, ECG, pulse oximetry, urinalysis, full blood count, electrolytes (especially potassium), urea/creatinine and infection markers.
Confirming cortisol excess: endocrinology may use late-night salivary cortisol, 24-hour urinary free cortisol or an overnight low-dose dexamethasone suppression test. Acute stress and exogenous steroids can distort results.
Localising the source: ACTH, pituitary MRI, adrenal CT or other imaging is performed after biochemical confirmation and specialist review.
Complication tests: blood cultures, chest imaging, troponin, CT pulmonary angiography/ultrasound when thromboembolism is suspected, bone imaging after trauma and visual-field testing for pituitary disease.
Do not delay emergency treatment while waiting for endocrine tests when the patient has sepsis, shock, dysrhythmia, pulmonary embolism, hypertensive emergency or severe hyperglycaemia.

Immediate management of common complications

Complication	Emergency priorities	Important caution
Sepsis/infection	ABCDE, cultures where possible, prompt antimicrobial pathway, fluids/vasopressors if shock and source control.	Steroid immunosuppression may blunt fever and inflammatory signs.
Hypertensive emergency	Monitor ECG, BP and neurological status; urgent medical treatment using controlled IV antihypertensives.	Do not rapidly lower BP without a monitored protocol.
Hyperglycaemia/DKA	Check glucose/ketones, ABCDE, fluids and urgent DKA pathway.	Never assume steroid-related hyperglycaemia is harmless.
Hypokalaemia	ECG monitoring, repeat potassium/magnesium and cautious replacement according to local protocol.	Renal impairment and digoxin use increase arrhythmia risk.
VTE/PE	Oxygen for hypoxaemia, urgent imaging/anticoagulation decision and critical-care escalation.	Assess bleeding risk, recent surgery and fracture before anticoagulation.
Psychosis/suicidality	Calm environment, remove hazards, one-to-one observation and mental-health emergency assessment.	Do not dismiss new psychiatric symptoms as “just steroid mood.”

Hospital and definitive management

Exogenous steroids: the prescriber/endocrinologist plans gradual dose reduction or conversion to physiologic replacement; abrupt cessation is unsafe after prolonged exposure.
Pituitary Cushing disease: transsphenoidal pituitary surgery is commonly first-line when appropriate; persistent disease may require medication, radiation or further surgery.
Adrenal or ectopic cortisol source: specialist surgery, oncological treatment or cortisol-lowering medicines may be required.
Medical cortisol control: endocrine teams may use steroidogenesis inhibitors or glucocorticoid-receptor antagonism with close liver, electrolyte, ECG and cortisol monitoring.
Treat hypertension, diabetes, osteoporosis, infection and psychiatric complications in parallel; do not wait for definitive tumour treatment.
After treatment of endogenous Cushing syndrome, the hypothalamic-pituitary-adrenal axis may remain suppressed. Steroid replacement and stress-dose planning may be necessary until recovery is documented.

Nursing and EMT interventions

Trend vital signs, glucose, potassium, mental state, pain, fluid balance, temperature and infection signs.
Use falls and fracture precautions; provide assistance with transfers, toileting, bathing and stair use.
Inspect skin and pressure areas, use gentle handling, support wound care and report cellulitis, thrush or delayed healing.
Administer medicines exactly as prescribed, double-check steroid route/dose and document the last dose and missed doses.
Provide nutrition advice through the clinical team: adequate protein, calcium/vitamin D when appropriate, moderated sodium and glucose-conscious meals.
Use therapeutic communication; screen for depression, mania, psychosis and suicidal thinking and escalate immediately when risk is present.
Teach the patient to carry a steroid emergency card/medical alert and a written sick-day plan when adrenal suppression is possible.

Complications and prevention

Prevent infection through vaccination review, hand hygiene, early wound assessment and prompt treatment of fever or respiratory symptoms.
Prevent VTE through risk assessment, mobilisation when safe, hydration and prescribed prophylaxis.
Reduce fracture risk with fall prevention, bone-density review and safe lifting; never encourage strenuous exercise during severe proximal weakness.
Monitor BP, glucose, potassium, lipids, weight, eyes, kidneys and mental health during long-term treatment.
Do not share steroid medicines, use potent creams without advice or stop chronic steroids suddenly.

Clinical scenarios

Scenario 1 — Infection hidden by steroids: A patient on long-term prednisolone has mild temperature elevation, confusion, tachycardia and a painful leg wound. Do not be reassured by the modest fever. Perform ABCDE, check glucose/lactate, obtain cultures where possible, start the sepsis pathway and arrange urgent hospital care.

Scenario 2 — Hypokalaemic weakness: A patient with rapid Cushingoid features has muscle weakness, BP 190/120 and palpitations. Place on ECG monitoring, check potassium/glucose/renal function, assess for hypertensive emergency and arrange urgent medical/endocrine review. Do not give potassium blindly or treat the BP with an unmonitored rapid drop.

Scenario 3 — Steroid withdrawal: A patient abruptly stops months of dexamethasone and develops vomiting, abdominal pain, profound weakness, hypotension and confusion. Suspect adrenal crisis, not “Cushing relapse.” Activate resuscitation, obtain cortisol/ACTH if this does not delay care, give emergency hydrocortisone and isotonic saline/dextrose under protocol, and transfer urgently.

Common errors to avoid

Diagnosing Cushing syndrome from body shape alone without reviewing steroids and confirming cortisol excess.
Stopping prescribed glucocorticoids abruptly or withholding stress-dose treatment in a seriously ill steroid-dependent patient.
Missing sepsis, pulmonary embolism, fracture, stroke, DKA, hypokalaemia or psychiatric emergency because symptoms are attributed to cortisol.
Using a random cortisol level as a stand-alone diagnostic test during acute stress.
Ignoring inhaled, topical, injected, traditional or “beauty” steroid products in the medication history.

CORTISOL SAFE: C — Check steroid exposure; O — Observe airway, breathing and circulation; R — Recognise infection/VTE/BP/glucose danger; T — Test glucose, potassium and ECG; I — Involve endocrine/medical teams; S — Support skin, bones and mental health; O — Omit no steroid abruptly; L — Link the patient to follow-up; S — Sick-day and steroid-alert education; A — Assess adrenal crisis after withdrawal; F — Falls/fracture precautions; E — Escalate deterioration.

Revision questions

Differentiate Cushing syndrome from Cushing disease and list common exogenous steroid sources.
Explain how cortisol excess causes hypertension, hyperglycaemia, hypokalaemia, infection and osteoporosis.
Which emergency findings require immediate transfer in a patient with suspected Cushing syndrome?
Why can steroid withdrawal produce adrenal crisis?
List the key questions in a steroid medication history.
Outline the EMT priorities for Scenario 1 and Scenario 3.

Key takeaways

Cushing syndrome is a chronic cortisol-excess state with acute complications. Treat the immediate emergency, search actively for infection, thromboembolism, hypertension, glucose and potassium problems, document every steroid exposure, and never stop long-term glucocorticoids abruptly.

References for further study

NIDDK. Cushing’s Syndrome — causes, diagnosis and definitive treatment.
Endocrine Society. Primary Adrenal Insufficiency Guideline Resources — immediate treatment principles for adrenal crisis.
Endocrine Society/ESE. Glucocorticoid-Induced Adrenal Insufficiency Guideline, 2024.
NHS. Cushing’s syndrome — clinical overview and long-term risks.
Use current Uganda Ministry of Health, hospital and endocrine protocols for steroid tapering, adrenal crisis, hypertension, infection and thromboembolism.

Cushing Syndrome: Recognition, Assessment and Emergency Management Read More »

Diabetic Ketoacidosis (DKA): Emergency Recognition, Assessment and Management

Why this topic matters: Diabetic ketoacidosis is a time-critical metabolic emergency caused by inadequate effective insulin, increased counter-regulatory hormones and accumulation of acidic ketones. It can develop in type 1 or type 2 diabetes, during pregnancy, after infection, trauma, surgery or missed insulin, and sometimes with only modest glucose elevation. DKA causes dehydration, potassium shifts, shock, dysrhythmias, cerebral injury and death unless fluids, insulin, electrolytes and the precipitating illness are treated in a monitored hospital setting.

Learning objectives

Explain the pathophysiology and diagnostic triad of hyperglycaemia or known diabetes, ketonaemia and metabolic acidosis.
Recognise early symptoms, severe DKA, euglycaemic DKA and dangerous complications.
Perform a rapid ABCDE assessment, bedside glucose/ketone testing, focused history and severity triage.
Describe safe pre-hospital stabilisation and the hospital sequence of fluids, insulin, potassium, dextrose and monitoring.
Identify common precipitants, special populations, treatment complications and prevention strategies.

Definition and pathophysiology

DKA occurs when there is too little effective insulin for the body’s needs, together with excess glucagon, adrenaline, cortisol and growth hormone. Glucose cannot be used adequately by cells, so the liver increases glycogenolysis and gluconeogenesis. At the same time, fat is broken down into free fatty acids; the liver converts them into beta-hydroxybutyrate and acetoacetate. These ketones consume bicarbonate and produce a high-anion-gap metabolic acidosis.

High glucose exceeds the renal reabsorption threshold and causes osmotic diuresis. Water and electrolytes (sodium, chloride, potassium, phosphate and magnesium) are lost through urine. Vomiting and reduced intake intensify the deficit. Serum potassium may initially be normal or high because acidosis and insulin deficiency shift potassium out of cells, even though total-body potassium is depleted. When insulin and fluids are started, potassium moves back into cells and the serum level can fall rapidly.

Diagnostic concept

Component	What to look for	Important caution
Diabetes/hyperglycaemia	Known diabetes or raised plasma/capillary glucose; many patients have marked hyperglycaemia.	Euglycaemic DKA can occur with SGLT2 inhibitors, pregnancy, fasting, vomiting or partial insulin treatment.
Ketonaemia	Raised blood beta-hydroxybutyrate or urine ketones; blood ketones reflect current physiology more reliably.	Urine strips may lag behind improvement because they measure acetoacetate rather than beta-hydroxybutyrate.
Metabolic acidosis	Low venous pH and/or bicarbonate, often with an increased anion gap.	Mixed disorders are common; sepsis, lactic acidosis and renal failure may coexist.
Clinical dehydration	Thirst, polyuria, dry mucosa, tachycardia, postural symptoms, weak pulses, hypotension or oliguria.	Normal blood pressure does not exclude a large deficit because compensation may be present.

Common precipitants

Insulin omission or interruption: missed doses, wrong dose, vomiting, insulin pump blockage, empty/expired insulin, poor injection technique or inability to obtain medicines.
Infection: pneumonia, urinary infection, skin/soft-tissue infection, malaria, gastroenteritis, tuberculosis or sepsis.
Acute physiological stress: myocardial infarction, stroke, pancreatitis, trauma, burns, surgery or severe asthma.
Medicines: corticosteroids, sympathomimetics, atypical antipsychotics and SGLT2 inhibitors.
New diabetes: first presentation of type 1 diabetes, especially in a child or young adult, or ketosis-prone type 2 diabetes.
Pregnancy and fasting: accelerated starvation and altered metabolism can produce DKA with lower glucose.
Psychosocial factors: fear of hypoglycaemia, eating disorder, depression, cognitive impairment, substance use, homelessness or lack of family support.

Clinical features and progression

Stage/pattern	Typical findings	Emergency significance
Early ketosis	Thirst, polyuria, nocturia, fatigue, headache, nausea, abdominal discomfort and rising glucose/ketones.	Early sick-day intervention may prevent progression; do not wait for coma.
Established DKA	Vomiting, dehydration, tachycardia, postural dizziness, weight loss, fruity breath, abdominal pain and deep rapid breathing.	Needs urgent hospital admission, IV access and serial biochemical monitoring.
Severe DKA	Hypotension/shock, oliguria, hypothermia, severe acidosis, altered mental status, seizures or coma.	High-dependency/ICU assessment; search for sepsis, infarction, cerebral injury and dysrhythmia.
Euglycaemic DKA	Ketones and acidosis with only modest glucose elevation.	Can be missed if clinicians rule out DKA because the glucose is not very high.

Red flags for immediate escalation: GCS falling, Kussmaul breathing with exhaustion, systolic hypotension, shock, severe abdominal pain, persistent vomiting, potassium-related ECG changes, anuria, pregnancy, renal/heart failure, suspected sepsis, cerebral symptoms or ketones above 3.0 mmol/L.

First contact and scene management

Use standard precautions and assess for vomit, sharps, insulin needles, pump equipment, alcohol, medicines and other hazards.
Identify the patient, introduce yourself and ask relatives to bring the insulin, diabetes card, glucose/ketone meter, medication list and sick-day plan.
Activate emergency transport and senior clinical support early. DKA is not safely managed at home or in an unmonitored clinic.
Keep the patient resting; prevent exertion. If vomiting, use a safe lateral position while protecting the airway and considering spinal/trauma precautions.
Do not give oral food or fluids to a drowsy, actively vomiting or aspiration-risk patient. A fully alert patient may take small sips while transfer is arranged unless fluid restriction applies.

ABCDE assessment

A — Airway

Assess speech, secretions, vomit, airway reflexes and ability to protect the airway. Reduced consciousness in DKA is a serious finding.
Suction, position and use basic airway adjuncts as trained. Prepare advanced airway support if airway protection fails.

B — Breathing

Count respiratory rate and assess depth, effort and Kussmaul pattern. A falling respiratory rate in an exhausted patient may signal impending respiratory failure, not improvement.
Measure SpO₂ and give oxygen for hypoxaemia or respiratory distress according to local protocol. Do not suppress compensatory hyperventilation without expert help.

C — Circulation

Measure pulse, blood pressure, capillary refill, temperature, peripheral perfusion and urine output. Check for shock and fluid overload risk.
Insert a large-bore IV cannula if trained; collect venous blood for glucose, ketones, electrolytes, urea/creatinine, full blood count, blood gas and cultures when indicated.
Begin isotonic crystalloid only under the local DKA protocol. Use smaller aliquots and close reassessment in heart failure, kidney failure, elderly patients and pregnancy.

D — Disability

Record AVPU/GCS, pupils, behaviour and focal neurological signs. Check capillary glucose and blood ketones immediately.
Confusion or coma may be due to acidosis, hyperosmolality, hypoglycaemia from treatment, stroke, sepsis, intoxication or cerebral oedema; never assume one cause.

E — Exposure

Check temperature, skin, injection sites, pump tubing, feet, wounds, pressure areas and signs of infection or trauma.
Look for pregnancy, dehydration, abdominal tenderness, chest pain, focal neurological deficit and medication interruption while preserving warmth and dignity.

Focused history: SAMPLER plus sick-day questions

Area	Questions
Symptoms and timeline	Thirst, urination, weight loss, nausea, vomiting, pain, fever, breathlessness, drowsiness and onset; how quickly are symptoms changing?
Diabetes	Type, duration, usual glucose/ketone values, previous DKA, hypoglycaemia awareness, pregnancy and complications.
Insulin and medicines	Name, dose, time of last dose, missed/extra dose, injection site, storage, pump function, steroids, SGLT2 inhibitor or new medicines.
Intake and losses	Last meal, fluid intake, vomiting/diarrhoea, fasting, alcohol, exercise and urine volume.
Precipitant screen	Cough, dysuria, malaria symptoms, wounds, chest pain, abdominal pain, surgery, trauma, pregnancy, stroke or mental-health crisis.
Allergies/social support	Allergies, access to insulin and strips, health literacy, family supervision and ability to follow a sick-day plan.

Investigations and interpretation

Glucose: repeat bedside value and send venous plasma glucose. Do not exclude DKA because the glucose is only modestly elevated.
Ketones: use blood beta-hydroxybutyrate when available. NHS guidance treats blood ketones over 3 mmol/L or urine ketones over 2+ as a medical emergency; local pathways may differ.
Venous blood gas: pH, bicarbonate, pCO₂ and lactate; calculate the anion gap when appropriate. Arterial sampling is reserved for specific respiratory/critical-care indications.
Electrolytes/renal function: sodium, potassium, chloride, bicarbonate, urea, creatinine, magnesium and phosphate; calculate corrected sodium and osmolality with senior input.
Precipitant tests: full blood count, cultures, urinalysis, malaria test where relevant, ECG/troponin, chest imaging, pregnancy test, lipase or other targeted tests.
Monitoring baseline: weight if safe, fluid balance, urine output, temperature, neurological status and medication reconciliation.

Immediate pre-hospital and emergency-department priorities

Recognise DKA early, call the receiving facility and communicate the glucose, ketones, mental state, vital signs, suspected cause and treatment already given.
Protect airway and breathing; position safely, suction vomit and give oxygen only when indicated by hypoxaemia or respiratory compromise.
Obtain IV access and collect blood without delaying circulation support. Treat shock with isotonic crystalloid under protocol and reassess after each bolus.
Do not give an insulin bolus or start an unsupervised infusion in the field unless a written local protocol, monitoring, pump and trained prescriber support it.
Transfer urgently to a facility able to measure electrolytes/ketones, provide IV insulin and manage dysrhythmias, renal failure, pregnancy or critical deterioration.

Hospital treatment sequence

The treatment aims are: restore perfusion, clear ketones, correct electrolyte deficits safely, reduce glucose without causing hypoglycaemia, treat the precipitating illness and prevent complications.

1. Fluids

Isotonic crystalloid is usually started first to restore intravascular volume and renal perfusion. JBDS notes that fluid replacement precedes insulin and aims to restore circulation, clear ketones and correct electrolyte imbalance.
Use the local adult protocol for rate and volume. Reassess blood pressure, pulse, urine output, lung sounds, sodium and osmolality frequently.
Modify fluid volume/rate in heart failure, renal failure, older adults, pregnancy and adolescents; excessive fluid can cause pulmonary oedema or neurological harm.

2. Insulin

Once initial fluids are running and potassium is known/managed, start a fixed-rate IV soluble insulin infusion in a monitored setting. JBDS commonly uses 0.1 units/kg/hour; the actual order must follow local policy.
Insulin suppresses ketogenesis; it is continued until ketones/acidosis resolve, not merely until glucose becomes normal.
When glucose falls below approximately 14 mmol/L in the JBDS pathway, add 10% dextrose and consider reducing insulin to 0.05 units/kg/hour to prevent hypoglycaemia and hypokalaemia while ketones clear.

3. Potassium and other electrolytes

Measure potassium before insulin and repeat frequently. Total-body potassium is depleted even when the admission serum value is high.
Do not add potassium when serum potassium is high or the patient is anuric; replace according to the result and local protocol. Severe hypokalaemia requires urgent senior/critical-care review before insulin.
Magnesium and phosphate may fall. Routine phosphate replacement is not recommended by JBDS, but specialist replacement may be considered for severe deficiency, respiratory weakness, cardiac dysfunction or rhabdomyolysis.

4. Dextrose and transition

Add IV dextrose when glucose falls while ketones remain, so insulin can continue to clear ketones safely.
Continue IV insulin and dextrose until the patient is clinically improved, ketones have cleared, acidosis has resolved and oral intake is reliable.
Start subcutaneous basal/bolus insulin before stopping IV insulin, with an overlap period specified by the hospital protocol, to avoid rebound ketosis.

Targets and monitoring in a monitored unit

Parameter	What to monitor	Why
Glucose	Hourly or according to the local pathway.	Detects treatment response, hypoglycaemia and the need for dextrose.
Ketones	Usually hourly when blood beta-hydroxybutyrate is available.	Confirms that ketogenesis is resolving; glucose alone is insufficient.
Vital signs/neurology	Pulse, BP, respiratory rate/depth, SpO₂, temperature and GCS at least hourly in severe illness.	Detects shock, respiratory fatigue, infection, cerebral oedema and fluid overload.
Electrolytes/acid–base	Venous pH/bicarbonate, potassium, sodium, urea/creatinine and osmolality at protocol intervals.	Guides insulin, potassium and fluid changes; identifies dangerous shifts.
Fluid balance	Every fluid, emesis, urine output and body weight when safe.	Measures resuscitation and prevents overload or persistent deficit.

DKA resolution and escalation

Use local biochemical criteria. JBDS defines resolution as blood ketones below 0.6 mmol/L and venous pH above 7.3; bicarbonate alone may be misleading after large volumes of saline.
Escalate to HDU/ICU for severe acidosis, shock, altered consciousness, severe potassium abnormality, respiratory failure, anuria, pregnancy, renal/heart failure, sepsis or inability to provide required monitoring.
If ketones are not falling at the expected rate, check the infusion pump, line, insulin preparation, fluid delivery, sampling accuracy, ongoing infection and missed diagnosis.
If consciousness deteriorates, reassess airway, glucose, sodium/osmolality, cerebral oedema, stroke, seizure, sepsis and other causes; urgent senior review and imaging may be required.

Complications of DKA and its treatment

Hypokalaemia: insulin and correction of acidosis drive potassium intracellularly; weakness, ECG changes, ventricular dysrhythmia and arrest can occur.
Hyperkalaemia: acidosis, renal failure and tissue breakdown can cause life-threatening conduction abnormalities before treatment.
Hypoglycaemia: occurs when insulin continues without timely dextrose or monitoring.
Cerebral oedema/neurological injury: more common in children and young people but neurological deterioration in any patient is an emergency.
Pulmonary oedema: excessive fluid in renal or cardiac failure; monitor crackles, oxygenation, work of breathing and weight.
Thrombosis, aspiration, acute kidney injury, rhabdomyolysis and myocardial injury: result from dehydration, inflammation, immobility or electrolyte shifts.
Hyperchloraemic acidosis: may persist after ketones resolve following large volumes of 0.9% saline; interpret the whole clinical and biochemical picture.

Special populations

Pregnancy: DKA can develop faster and at lower glucose. Treat as an obstetric emergency with medical, diabetes and obstetric teams; monitor mother and fetus.
Children/adolescents: use a paediatric pathway, weight-based fluid calculation and specialist support; do not apply adult boluses or infusion rates.
Renal failure/dialysis: volume, potassium and insulin clearance differ; avoid routine large fluid loads and involve nephrology/critical care.
Heart failure/older adults: give smaller aliquots with frequent lung, perfusion and urine reassessment.
SGLT2 inhibitors: consider euglycaemic DKA during illness, fasting, surgery or reduced insulin; check ketones even when glucose is not very high.

Nursing and EMT responsibilities

Use a DKA observation chart; document every glucose, ketone, electrolyte, infusion rate, fluid volume, urine output, neurological score and clinical response.
Check IV lines, insulin pump settings, infusion-pump programming and dextrose/potassium compatibility with an independent second checker where policy requires.
Maintain aspiration, seizure, falls and pressure-injury precautions; provide oral care and reposition safely.
Monitor for infection, chest pain, ECG changes, abdominal deterioration, worsening work of breathing, fluid overload and reduced urine output.
Explain procedures calmly, involve family with consent, provide culturally appropriate education and use teach-back to confirm understanding.
Escalate any unexpected trend rather than waiting for the next scheduled sample. A falling glucose with persistent ketones is not treatment failure if insulin and dextrose are being used correctly; a rising ketone level is concerning.

Discharge planning and prevention

Identify and address the precipitant: infection treatment, insulin access, pump education, medicine reconciliation, mental-health support or diabetes-team review.
Confirm the patient can eat and drink, administer insulin correctly, recognise hypo/DKA symptoms and access glucose/ketone testing.
Provide a written sick-day plan: continue prescribed basal insulin, check glucose frequently, test ketones during illness/high readings, maintain fluids if safe and seek help early.
Explain never to stop insulin simply because food intake is reduced; obtain professional advice for dose adjustment.
Arrange diabetes specialist and primary-care follow-up, review injection sites and technique, and assess social barriers, literacy and family support.

Clinical scenarios

Scenario 1 — Missed basal insulin: A 19-year-old with type 1 diabetes has thirst, vomiting, abdominal pain, glucose 28 mmol/L, blood ketones 5.2 mmol/L and deep respirations. Treat as severe DKA: ABCDE, IV access, isotonic fluid under protocol, urgent transfer to monitored care, blood gas/electrolytes and specialist insulin pathway. Never give oral fluids to a drowsy vomiting patient.

Scenario 2 — Euglycaemic DKA: A patient taking an SGLT2 inhibitor has nausea and rapid breathing after fasting for illness. Glucose is 9.8 mmol/L but ketones are 4.0 mmol/L and pH is low. DKA remains possible; stop the suspected precipitant under medical direction, begin emergency assessment and transfer for IV fluids, dextrose/insulin and electrolyte management.

Scenario 3 — DKA with renal failure: An older patient on dialysis is hypotensive but has crackles and potassium 6.4 mmol/L. Do not apply a routine large fluid bolus. Give cautious resuscitation with senior/renal/critical-care involvement, continuous ECG monitoring and urgent hyperkalaemia treatment while confirming DKA.

Common errors to avoid

Ruling out DKA because glucose is below 14 mmol/L or because the patient has type 2 diabetes.
Starting insulin before checking potassium, perfusion and the local monitored protocol.
Stopping insulin as soon as glucose normalises while ketones/acidosis persist.
Using bicarbonate routinely, replacing phosphate routinely or giving potassium without a result and urine assessment.
Giving large fluid volumes without reassessing lungs, urine output, sodium/osmolality, heart failure or kidney failure.
Missing infection, myocardial infarction, pregnancy, SGLT2 medicine use, pump failure or social barriers as the trigger.

KETONES SAFE: K — Keep airway and circulation safe; E — Examine glucose, ketones and electrolytes; T — Treat dehydration with monitored crystalloid; O — Observe neurological state and urine output; N — Never stop insulin solely because glucose falls; E — Electrolyte potassium plan; S — Search and treat the precipitant; S — Specialist referral; A — Add dextrose when needed; F — Follow ketone/pH trends; E — Educate before discharge.

Revision questions

Describe how insulin deficiency produces ketones, acidosis, osmotic diuresis and total-body potassium loss.
What three biochemical components support a diagnosis of DKA?
Why can a patient with euglycaemic DKA be missed?
List six precipitants and explain how the history may identify each one.
Why is potassium checked before insulin, and why can it fall rapidly during treatment?
What are the indications for adding IV dextrose while continuing insulin?
Write a structured handover for Scenario 2, including the urgency and key treatment already given.

Key takeaways

DKA is a ketone-and-acid emergency, not simply a high-glucose problem. Recognise it early, assess ABCDE, measure glucose and ketones, restore perfusion carefully, manage potassium before insulin, continue insulin until ketones clear, treat the trigger and monitor continuously.

References for further study

Umpierrez et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report. Diabetes Care, 2024.
Joint British Diabetes Societies. The Management of Diabetic Ketoacidosis in Adults, current 2023 guideline.
NHS. Diabetic ketoacidosis — symptoms, ketone thresholds, urgent referral and sick-day prevention.
NICE Clinical Knowledge Summaries. When to suspect hyperglycaemic emergencies.
Follow current Uganda Ministry of Health, hospital and specialist protocols for adult, paediatric, pregnancy and renal-failure DKA.

Diabetic Ketoacidosis (DKA): Emergency Recognition, Assessment and Management Read More »

Hypoglycaemia and Hyperglycaemia: Emergency Recognition, Assessment and Management

Why this topic matters: Glucose disturbances can injure the brain, heart and kidneys within minutes. Hypoglycaemia may progress from sweating and confusion to seizures, coma and death; hyperglycaemia may signal dehydration, diabetic ketoacidosis (DKA), hyperosmolar hyperglycaemic state (HHS), infection or another life-threatening stress. Emergency medical technicians must measure glucose early, protect the airway, treat the immediate threat, search for the cause, reassess response and arrange safe referral.

Learning objectives

Define hypoglycaemia and hyperglycaemia using clinically useful glucose ranges and explain why symptoms may not match the number.
Recognise autonomic, neuroglycopenic, dehydration and metabolic signs of glucose emergencies.
Perform a glucose-focused ABCDE assessment, including safe capillary sampling, AVPU/GCS and ketone screening.
Give safe first aid to a conscious patient and emergency treatment to a patient who cannot swallow.
Differentiate uncomplicated hyperglycaemia from DKA, HHS, sepsis, stroke, intoxication and other causes of altered consciousness.
Describe pre-hospital, emergency-department, nursing, monitoring, documentation, discharge and prevention priorities.

Glucose physiology and key definitions

Glucose is the principal fuel for the brain and an important substrate for muscle and other tissues. Insulin moves glucose into cells and suppresses hepatic glucose output. Counter-regulatory hormones (glucagon, adrenaline, cortisol and growth hormone) raise glucose during fasting or stress. Diabetes occurs when insulin production is deficient, insulin action is inadequate, or both; uncontrolled diabetes produces persistent hyperglycaemia and can damage blood vessels, nerves, eyes, heart and kidneys.

Hypoglycaemia is clinically important low glucose. In most adults with diabetes, a reading below 4.0 mmol/L (70 mg/dL) should be treated when symptoms are present. ADA terminology commonly describes level 1 as <3.9 mmol/L, level 2 as <3.0 mmol/L (54 mg/dL), and level 3 as severe hypoglycaemia requiring help from another person, regardless of the measured value. Local protocols may use slightly different thresholds.

Hyperglycaemia means glucose above the person’s target range. A single high reading is not automatically DKA or HHS. It becomes an emergency when accompanied by ketones, acidosis, severe dehydration, altered mental status, shock, vomiting, infection or rapidly worsening illness. DKA and HHS are covered here as recognition-and-stabilisation priorities; definitive insulin and electrolyte protocols require a trained hospital team.

Useful glucose ranges and clinical interpretation

Finding	Approximate adult value	Clinical meaning and action
Low glucose / treat as hypo	<4.0 mmol/L (70 mg/dL)	Confirm with a repeat sample if the result does not fit the patient, but do not delay treatment in a symptomatic or deteriorating patient.
Clinically significant low level	<3.0 mmol/L (54 mg/dL)	High risk of neuroglycopenia, seizure and coma; give rapid glucose and investigate the cause.
Normal fasting range	Approximately 3.9–5.5 mmol/L	Interpret with meals, medicines, pregnancy, age and the patient’s usual target.
Hyperglycaemia	Above the person’s target; often >7 mmol/L fasting or >11 mmol/L random	Repeat, assess symptoms and check ketones when illness, type 1 diabetes or marked elevation is present.
Possible DKA/HHS	Often >13.9 mmol/L (250 mg/dL), but DKA can be euglycaemic	Look for ketones, vomiting, abdominal pain, deep breathing, dehydration, hypotension or altered consciousness; transfer urgently.

Causes and risk factors for hypoglycaemia

Excess medication: too much insulin, wrong insulin, duplicate dose, sulfonylurea (for example glibenclamide/gliclazide) or an unrecognised medication interaction.
Insufficient intake: missed or delayed meal, vomiting, diarrhoea, fasting, swallowing difficulty, food insecurity or a child who refuses food.
Increased use: strenuous work, exercise, prolonged walking, seizures or increased metabolic demand without carbohydrate adjustment.
Alcohol: especially binge drinking or alcohol taken without food; delayed hypoglycaemia can occur hours later because hepatic glucose production is impaired.
Organ failure: renal or hepatic impairment slows insulin and medicine clearance and reduces glucose production.
Critical illness: sepsis, severe malaria, starvation, adrenal insufficiency, hypopituitarism or advanced heart failure.
Endocrine and rare causes: insulinoma, non-islet-cell tumours, reactive hypoglycaemia and inherited metabolic disease.

Causes and risk factors for hyperglycaemia

Missed insulin or diabetes medicines, incorrect injection technique, expired insulin or interruption of an insulin pump.
Infection, myocardial infarction, stroke, trauma, surgery, burns, pancreatitis and other catecholamine-stressed states.
Excess carbohydrate intake, dehydration, sedentary behaviour or inability to access medicines.
Corticosteroids, some antipsychotics, thiazides, sympathomimetics and enteral/parenteral nutrition.
New-onset diabetes, pregnancy-related diabetes, pancreatic disease or endocrine excess such as Cushing syndrome or thyroid storm.
Reduced insulin action in severe obesity, renal or hepatic disease, or during acute illness.

Clinical features of hypoglycaemia

Physiological response	Typical findings	Why it matters
Adrenergic/autonomic	Sweating, tremor, palpitations, anxiety, hunger, tingling lips, pallor and irritability.	Warns the patient early and is driven by adrenaline; beta-blockers may mask tachycardia and tremor.
Neuroglycopenic	Headache, blurred vision, weakness, poor concentration, slurred speech, confusion, abnormal behaviour, ataxia, drowsiness.	The brain is not receiving enough glucose. Treat promptly and do not label the patient as intoxicated or psychiatric without checking.
Severe	Seizure, coma, inability to swallow, focal-looking neurological signs or cardiac dysrhythmia.	Protect airway, call for advanced help, give parenteral glucose/glucagon and search for another cause if recovery is incomplete.

Clinical features of hyperglycaemia and dehydration

Polyuria, polydipsia, nocturia, dry mouth, thirst, fatigue, blurred vision, weight loss and recurrent infections.
Dehydration signs: tachycardia, postural dizziness, delayed capillary refill, weak pulses, poor skin turgor and hypotension.
DKA clues: nausea, repeated vomiting, abdominal pain, fruity/acetone breath, deep rapid Kussmaul breathing, dehydration and progressive drowsiness.
HHS clues: profound dehydration, very high glucose, weakness, visual change, confusion, focal deficit, seizures or coma; ketosis may be mild or absent.
Always look for a precipitant: fever, cough, dysuria, wound, chest pain, neurological deficit, medication interruption or pregnancy.

High-risk rule: An abnormal mental state is never explained by “diabetes” alone. Check airway, oxygenation, glucose, temperature, blood pressure, stroke signs, trauma, sepsis and poisoning. A normal glucose does not exclude DKA, stroke, sepsis or another emergency.

First contact and scene priorities

Use standard precautions; check the scene for sharps, vomit, medicines, alcohol, pesticides and other hazards.
Introduce yourself, obtain consent where possible and ask a bystander to bring the patient’s diabetes card, insulin, medicines, glucose meter and glucagon kit.
Look for medical-alert jewellery, insulin pens, syringes, glucose tablets, ketone strips, an insulin pump and a treatment plan.
Assess responsiveness and breathing immediately. If unresponsive and not breathing normally, activate resuscitation procedures rather than treating presumed hypoglycaemia alone.
Position a conscious vomiting patient safely; place an unconscious patient who is breathing normally in the recovery position unless trauma or spinal precautions require another approach.

ABCDE assessment for a glucose emergency

A — Airway

Check speech, gurgling, vomit, secretions, tongue obstruction and protective reflexes.
Suction as needed, use an appropriate airway manoeuvre and prepare advanced airway support if consciousness is falling.
Never put food, drink, gel or tablets into the mouth of a drowsy, seizing or unconscious person.

B — Breathing

Count rate, assess depth and pattern, listen for Kussmaul breathing and measure SpO₂.
Give oxygen for hypoxaemia or respiratory distress according to local protocol; do not use oxygen to mask poor perfusion or delay transfer.
Deep rapid breathing with hyperglycaemia suggests metabolic acidosis and requires urgent hospital assessment.

C — Circulation

Check pulse, blood pressure, capillary refill, temperature of extremities, hydration, urine history and signs of shock.
Establish IV access in severe hypoglycaemia, shock, suspected DKA/HHS or inability to swallow. Take blood for laboratory testing before fluids when this does not delay resuscitation.
Use isotonic crystalloid for clinically significant dehydration or shock under local protocol, with caution in heart or renal failure.

D — Disability

Record AVPU and, when indicated, GCS; check pupils, speech, limb power and seizure activity.
Measure bedside capillary glucose immediately. If the reading is unexpected, repeat with a clean, warm finger and check the meter/strip expiry.
Check blood or urine ketones when glucose is high, the patient is unwell, type 1 diabetes is present or DKA is possible.

E — Exposure and examination

Measure temperature, inspect injection sites, pump tubing, skin infection, pressure injuries, feet, wounds and signs of trauma.
Look for infection, dehydration, pregnancy, alcohol or drug use and evidence of neglect or inability to obtain food/medicine.
Maintain dignity and warmth; record all findings and response to treatment.

Focused history: SAMPLE plus glucose questions

History area	Questions for the patient, family or records
Symptoms/onset	When did sweating, confusion, thirst, vomiting or breathlessness begin? Sudden or gradual? Better after food?
Diabetes details	Type 1, type 2, gestational or no known diabetes? Usual readings? Last meal? Usual hypo warning symptoms? Previous DKA/HHS?
Medication	Insulin name, dose, timing and site; tablets; steroids; last dose; missed or duplicated doses; new medicines; pump interruption.
Intake and losses	Food and fluid intake, vomiting, diarrhoea, fasting, alcohol, exercise and access to clean water.
Precipitating illness	Fever, cough, dysuria, wounds, chest pain, abdominal pain, pregnancy, stroke symptoms, trauma or infection contact.
Events and treatment	What glucose was measured, what carbohydrate/glucagon/dextrose was given, when, by whom and with what response?

Investigations and point-of-care checks

Repeat capillary glucose after treatment and compare with a venous plasma sample when shock, oedema, severe dehydration, hypothermia or a peri-arrest state may make finger-stick readings unreliable.
Blood ketones (preferably beta-hydroxybutyrate) or urine ketones; venous/arterial blood gas for pH, bicarbonate and lactate in suspected DKA or shock.
Urea, creatinine, sodium, potassium, chloride, bicarbonate, magnesium and phosphate; renal impairment changes insulin and medicine clearance.
Full blood count, cultures when infection is suspected, urinalysis, ECG, troponin, chest radiograph or pregnancy test as clinically indicated.
Consider malaria testing in a febrile patient in Uganda, toxicology, cortisol, insulin/C-peptide or imaging when recurrent unexplained hypoglycaemia is present.

Management of a conscious, cooperative hypoglycaemic patient

Confirm the reading if possible, but treat immediately when symptoms strongly suggest a hypo and measurement is delayed.
Give approximately 15–20 g of fast-acting carbohydrate: glucose tablets/gel, a measured sugary drink or fruit juice. Avoid chocolate or high-fat food as the sole first treatment because absorption is slower.
Recheck glucose after 10–15 minutes. If it remains below 4.0 mmol/L or symptoms persist, repeat the fast carbohydrate.
Once recovered and above the treatment threshold, give a longer-acting carbohydrate snack or meal, especially if the next meal is more than an hour away or a long-acting insulin/sulfonylurea was involved.
Observe for recurrence, identify the cause and arrange clinical review when the episode was severe, recurrent, unexplained, nocturnal, alcohol-related or caused by a long-acting medicine.

Severe hypoglycaemia: patient cannot swallow, is seizing or unconscious

Call for advanced help, place the patient safely, protect from injury and manage airway/breathing. Do not give anything by mouth.
Obtain IV/IO access. Follow the facility protocol for IV glucose; a common adult approach is 10% glucose in small aliquots with repeat glucose checks, avoiding extravasation. RCUK describes 50 mL of 10% glucose initially in an unconscious adult, repeated as required up to 250 mL while monitoring response.
If IV access is delayed, give glucagon according to available product and local protocol (adult emergency kits commonly contain 1 mg IM/SC). Glucagon may be less effective in prolonged fasting, alcohol-related hypoglycaemia or severe liver disease.
Recheck glucose in about 10 minutes and after each treatment. Continue airway support and investigate other causes if consciousness does not improve promptly.
After recovery, give oral carbohydrate only when the swallow is clearly safe. Monitor for rebound hypoglycaemia, especially after sulfonylureas or long-acting insulin, and refer for observation.

Medication safety: Do not give an unconscious patient oral glucose, water, food or tablets. Do not inject insulin to treat a high reading before assessing ketones, hydration, potassium and the possibility of DKA/HHS. Follow Uganda Ministry of Health, facility and prescriber protocols for drug doses.

Initial management of hyperglycaemia without shock

Repeat the reading, assess symptoms, check ketones when indicated and ask why glucose rose (missed insulin, infection, steroid, pump failure or dietary change).
Encourage appropriate oral fluids only if the patient is alert, not vomiting and has no fluid restriction. Do not force oral fluids in a confused or aspirating patient.
Do not advise exercise when ketones, vomiting, dehydration or severe hyperglycaemia are present; activity can worsen ketosis.
Arrange same-day clinical review for persistent high readings, ketones, pregnancy, type 1 diabetes, recurrent vomiting or an uncertain diagnosis.
Transfer urgently for red flags: hypotension, tachycardia, Kussmaul breathing, abdominal pain, repeated vomiting, severe dehydration, altered consciousness, seizure, suspected infection or inability to take medicines.

Recognising DKA and HHS

Feature	DKA	HHS	Action for EMT
Typical setting	Often type 1 diabetes, but can occur in type 2, pregnancy or SGLT2-inhibitor use.	Often older or type 2 patient with infection, stroke, poor access to fluids or missed treatment.	Do not rely on diabetes type; check glucose, ketones, hydration and mental status.
Glucose	Usually elevated, but euglycaemic DKA is possible.	Usually very high, often ≥30 mmol/L (600 mg/dL).	High glucose alone cannot distinguish the two.
Ketones/acidosis	Prominent ketones and metabolic acidosis; fruity breath and Kussmaul breathing may occur.	Minimal ketones and little acidosis, although mixed presentations occur.	Check beta-hydroxybutyrate/urine ketones and venous blood gas.
Fluid loss	Moderate to severe dehydration from osmotic diuresis and vomiting.	Often profound dehydration with neurological symptoms.	IV isotonic fluid and urgent hospital-level monitoring are usually required.
Neurology	Alertness falls as acidosis worsens.	Confusion, focal deficits, seizures or coma may dominate.	Assess for stroke, sepsis and electrolyte derangement rather than attributing everything to glucose.

Hospital management principles for DKA/HHS

Move to a monitored area; repeat vital signs, neurological observations, glucose, ketones, electrolytes, renal function and acid–base measurements.
Restore circulating volume with isotonic crystalloid while reassessing blood pressure, urine output, lung sounds, sodium and cardiac/renal status.
Insulin is prescribed only after potassium and perfusion are assessed; insulin drives potassium into cells and can precipitate dangerous hypokalaemia.
Replace potassium and other electrolytes according to laboratory results and the hospital protocol; do not give potassium blindly.
Treat the precipitant: infection, myocardial infarction, stroke, medication omission, pump failure, pancreatitis or steroid exposure.
As glucose falls, dextrose may be added so insulin can continue until ketones and acidosis resolve. A “normal” glucose does not prove DKA is cured.
HHS requires careful correction of osmolality and fluid deficit; rapid shifts may cause neurological harm. Seek senior/critical-care input early.

Nursing and EMT interventions

Record time, glucose value, symptoms, treatment, dose, route, response and the person who administered it.
Reassess airway, respiratory pattern, mental status, pulse, blood pressure, temperature, hydration and glucose at a frequency matched to severity.
Maintain IV patency and inspect the site during dextrose administration; extravasation can cause tissue injury.
Measure input/output and urine output; report oliguria, worsening dehydration, pulmonary crackles or new oedema.
Use falls, seizure and aspiration precautions; keep suction, oxygen, airway equipment and emergency glucose available.
Check medication administration records, insulin timing, meal intake, renal function and changes in steroids or antimicrobials.
Communicate deterioration using SBAR and hand over the last glucose, ketone result, treatment and trend rather than a single number.

Complications to anticipate

Hypoglycaemia: seizures, aspiration, traumatic injury, dysrhythmias, myocardial ischaemia, permanent neurological injury and death.
Hyperglycaemia: severe dehydration, acute kidney injury, infection, thrombosis, electrolyte derangement, cerebral dysfunction and coma.
Treatment complications: IV extravasation, hypokalaemia during insulin therapy, fluid overload, cerebral oedema or overly rapid osmolality correction.
Recurrent or nocturnal episodes causing falls, fear of insulin, poor adherence and loss of hypoglycaemia awareness.

Prevention and patient education

Teach the patient and family the signs of a hypo, the 15–20 g fast-carbohydrate rule, the 10–15 minute recheck and when to use glucagon.
Carry glucose, a medical-alert card and emergency contact details; teach colleagues or family how to place the person safely and call for help.
Never omit basal insulin without professional advice; instead follow the sick-day plan, check glucose/ketones more often and seek review early.
Coordinate meals, insulin, exercise and alcohol. Avoid driving, heights or machinery until fully recovered and safe under local regulations.
Review injection sites, device technique, medicine storage, expiry dates, renal function and access barriers at follow-up.
Encourage healthy diet, regular activity when well, tobacco avoidance, blood-pressure control, foot care and routine screening for kidney, eye and nerve complications.

Clinical scenarios for EMT practice

Scenario 1 — “Drunk” at a taxi stage: A man is sweaty, confused and unsteady. His breath smells of alcohol and his glucose is 2.4 mmol/L. He can swallow. Give fast carbohydrate, recheck in 10–15 minutes, keep him supervised and arrange assessment because alcohol-related and recurrent hypoglycaemia may occur after initial recovery.

Scenario 2 — Unconscious insulin user: A woman is unresponsive but breathing normally; her family reports insulin use and a missed meal. Check glucose while managing ABCDE, place her safely, give IV/IO glucose or glucagon according to protocol, repeat the measurement, protect the airway and transfer even if she wakes because the insulin effect may persist.

Scenario 3 — High reading with deep breathing: A young adult with type 1 diabetes has glucose 24 mmol/L, vomiting, abdominal pain and deep rapid respirations. Treat as suspected DKA: oxygen if hypoxaemic, IV access, cautious isotonic fluid under protocol, ketones/venous gas, no oral intake if vomiting and urgent hospital transfer. Do not give unsupervised insulin or delay for a routine clinic appointment.

Common errors to avoid

Failing to check glucose in every patient with altered consciousness, seizure, collapse or unexplained aggression.
Giving oral food or drink to a drowsy patient, or assuming a normal first reading excludes a serious illness.
Treating the number without assessing the cause, ketones, hydration, potassium, infection and medication history.
Giving insulin for hyperglycaemia without a protocol, potassium result or a monitored setting.
Stopping assessment after the patient “wakes”; recurrence, stroke, sepsis, overdose or head injury may coexist.

HYPO SAFE: H — Hypoglycaemia check; Y — Your airway and breathing first; P — Protect from aspiration; O — Oral carbohydrate only if safe; S — Sugar recheck; A — Assess cause; F — Follow-up/food; E — Escalate severe or recurrent episodes.

Revision questions

What glucose threshold should prompt treatment of a symptomatic adult, and why should treatment not be delayed when the patient is deteriorating?
List five adrenergic and five neuroglycopenic features of hypoglycaemia.
Explain the difference between a patient who can safely swallow and one who requires IV glucose or glucagon.
Why can beta-blockers, renal failure and alcohol make hypoglycaemia harder to recognise or longer lasting?
Which findings suggest DKA or HHS rather than uncomplicated hyperglycaemia?
Why must potassium and perfusion be assessed before hospital insulin therapy?
Write an SBAR handover for the patient in Scenario 3.

Key takeaways

Measure glucose early, protect the airway, treat low glucose promptly, look for ketones and dehydration when glucose is high, reassess after every intervention, and always identify the underlying cause. Emergency care is not complete when the number improves; safe observation, documentation, referral and prevention are part of the treatment.

References for further study

American Diabetes Association. Standards of Care in Diabetes—2026: Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises.
Resuscitation Council UK. The ABCDE Approach — bedside glucose assessment and IV 10% glucose guidance.
NHS. Low blood sugar (hypoglycaemia) — symptoms, 15-minute treatment, glucagon and prevention.
World Health Organization. Diabetes fact sheet — physiology, symptoms, complications and prevention.
Use current Uganda Ministry of Health, facility and prescriber protocols for medication concentrations, paediatric doses, DKA/HHS pathways and referral.

Hypoglycaemia and Hyperglycaemia: Emergency Recognition, Assessment and Management Read More »

Tubulointerstitial Diseases: Recognition, Assessment and Emergency Management

Why this topic matters: Tubulointerstitial diseases injure the kidney tubules and surrounding interstitium. They may cause acute kidney injury, electrolyte and acid–base disorders, polyuria, impaired concentration, fever, rash or progressive chronic kidney disease. Acute interstitial nephritis is often medication-related and may be reversible when recognised early. Emergency providers must identify the trigger, stop avoidable exposure, assess dangerous complications and refer promptly.

Learning objectives

Differentiate acute interstitial nephritis, acute tubular injury and chronic tubulointerstitial disease.
Recognise AKI, electrolyte loss, acidosis, polyuria, obstruction and systemic red flags.
Take a complete medication, infection, toxin, occupational and family history.
Describe investigations, supportive care, medicine withdrawal and specialist treatment.
Plan nursing monitoring, prevention, discharge education and renal follow-up.

Definition and pathophysiology

The renal tubules reabsorb water and electrolytes, regulate acid-base balance and concentrate urine. The interstitium contains supporting tissue, blood vessels and immune cells. Tubulointerstitial disease disrupts these functions without necessarily causing heavy proteinuria or dramatic urine findings.

Acute tubulointerstitial nephritis (ATIN) is commonly an immune-mediated reaction to a drug, infection or systemic disease. Acute tubular injury/necrosis follows ischaemia, sepsis, toxins or pigment injury. Chronic tubulointerstitial nephritis develops from prolonged medicines, obstruction, reflux, metabolic disease, toxins, autoimmune disease or inherited disorders and may progress to CKD.

Causes and risk settings

Cause	Examples	Important clues
Medicines	Beta-lactam antibiotics, sulfonamides, NSAIDs, PPIs, diuretics, anticonvulsants, rifampicin and selected antivirals.	New medicine or dose change days to weeks before AKI, fever, rash or eosinophilia.
Ischaemia/sepsis	Shock, severe infection, burns, surgery or major blood loss.	Hypotension, lactate rise, oliguria and multi-organ dysfunction.
Toxins/pigment	Heavy metals, solvents, contrast, myoglobin and haemoglobin.	Occupational exposure, rhabdomyolysis, dark urine or haemolysis.
Infection/immune disease	Pyelonephritis, TB, HIV, sarcoidosis, lupus, Sjögren and vasculitis.	Fever, systemic symptoms, rash, pulmonary or joint disease.
Chronic structural/metabolic	Reflux, obstruction, stones, analgesic abuse, hypercalcaemia, hypokalaemia or cystic disease.	Polyuria, bland urine, concentrating defect and slowly falling eGFR.

Emergency red flags

Rapid creatinine rise, oliguria/anuria, hyperkalaemia, acidosis or pulmonary oedema.
Fever, diffuse rash, facial swelling, wheeze or hypotension after a medicine.
Severe polyuria with dehydration, hypernatremia or hypokalaemia.
Confusion, seizures, pericarditis, bleeding or other uraemic complications.
Sepsis, shock, rhabdomyolysis, haemolysis or suspected toxin exposure.
Pregnancy, child, transplant, solitary kidney or advanced CKD with new deterioration.

Triage and first contact

Place unstable patients in a monitored area; call senior emergency, renal, pharmacy and critical-care support.
Ask about every prescribed, over-the-counter, herbal and traditional medicine; record start/stop dates and dose.
Assess urine volume, thirst, nocturia, fever, rash, joint pain, infection, obstruction, workplace chemicals and recent contrast.
Perform ABCDE, glucose, ECG, BP, fluid-status assessment, skin examination and medication reconciliation.
Stop suspected non-essential nephrotoxins under prescriber guidance and arrange urgent renal referral for AKI or systemic disease.

ABCDE assessment

Step	Assess	Actions
A – Airway	Uraemic vomiting, confusion, seizures and aspiration risk.	Position, suction and airway support if consciousness is impaired.
B – Breathing	Crackles, hypoxia, Kussmaul breathing, pulmonary oedema or haemoptysis.	Oxygen for hypoxaemia and urgent fluid/renal/critical-care review.
C – Circulation	BP, perfusion, dehydration, oedema, arrhythmia and shock.	Carefully reassessed fluids or source control; continuous ECG for electrolyte risk.
D – Disability	Glucose, confusion, asterixis, seizures, weakness and tetany.	Check electrolytes, treat emergencies and reassess after intervention.
E – Exposure	Rash, fever, oedema, bruising, muscle tenderness and catheter/obstruction signs.	Identify trigger, prevent pressure injury and preserve dignity.

History and examination

Timeline of renal decline, urine output, thirst, nocturia, weight change and previous kidney function.
Medication history including antibiotics, NSAIDs, PPIs, diuretics, anticonvulsants, supplements and herbal remedies.
Recent infections, fever, rash, joint pain, sinus disease, autoimmune symptoms, TB/HIV risk and travel.
Shock, burns, surgery, trauma, contrast, muscle injury, strenuous exercise and heat exposure.
Examine volume status, lungs, heart, BP, skin, joints, muscle tenderness, abdomen, bladder and neurological function.

Investigations

Test	Purpose	Interpretation
Creatinine/eGFR, urea and electrolytes	Identify AKI, CKD, potassium and acid-base complications.	Trend results and adjust renally cleared medicines.
Urinalysis/microscopy	Detect blood, protein, leucocytes, casts and concentration defect.	WBCs or WBC casts may support interstitial inflammation; bland urine does not exclude disease.
FBC, eosinophils, CRP, cultures	Assess inflammation, infection and allergic reaction.	Eosinophilia is supportive but not required for ATIN.
CK, blood gas, glucose, calcium, phosphate and magnesium	Identify rhabdomyolysis, acidosis and electrolyte wasting.	Correct life-threatening abnormalities immediately.
Autoimmune, infection and toxin tests	Find systemic or exposure-related causes.	Use history to guide ANCA, ANA, complements, HIV/TB/hepatitis and toxicology.
Ultrasound/biopsy	Exclude obstruction and establish diagnosis when needed.	Biopsy is specialist-led after coagulation/BP review.

Immediate management

Stop the suspected offending medicine or toxin when safe and document the reaction in the medical record.
Treat sepsis, shock, obstruction, rhabdomyolysis and other reversible causes promptly.
Maintain euvolaemia; give fluid for true depletion and restrict/diurese clinically important overload under prescription.
Correct hyperkalaemia, acidosis, severe sodium/potassium loss and glucose disturbances.
Adjust all medicines for changing renal function and involve pharmacy/renal services.
Discuss renal replacement therapy for refractory potassium/acidosis, pulmonary oedema, uraemia or dialysable toxins.

Acute interstitial nephritis

ATIN often develops after a medicine exposure and may present with AKI, fever, rash, arthralgia, eosinophilia, pyuria or mild proteinuria. The classic triad is not present in every patient. Treatment begins with stopping the trigger and managing complications. Corticosteroids may be considered for immune-mediated or selected medication-related cases by a nephrologist, often after biopsy or careful assessment.

Review the medication timeline and identify the most likely culprit.
Stop non-essential suspected medicines; substitute essential treatment with specialist advice.
Monitor creatinine, urine output, potassium, BP, rash and systemic symptoms.
Exclude infection and obstruction before immunosuppression.
Arrange renal follow-up because recovery may be incomplete and CKD can develop.

Acute tubular injury and chronic disease

In ischaemic or septic tubular injury, restore perfusion, control infection, avoid further nephrotoxins and maintain euvolaemia.
Rhabdomyolysis requires early assessment of CK, potassium, calcium, acidosis and urine output, with carefully guided fluids.
Chronic tubulointerstitial disease may cause polyuria, nocturia, salt wasting, metabolic acidosis and progressive CKD.
Treat obstruction, metabolic causes, infection and occupational exposures; arrange nephrology follow-up and renal-dose medication review.

Electrolyte and acid-base emergencies

Hyperkalaemia: ECG, cardiac membrane stabilisation and potassium-shifting/removal protocol.
Hypokalaemia: replace potassium cautiously, check magnesium and investigate renal wasting; monitor ECG.
Metabolic acidosis: obtain blood gas, treat shock/sepsis and discuss bicarbonate or dialysis according to severity.
Hypernatremia/dehydration: replace water gradually and monitor neurological status.
Phosphate/calcium disturbances: assess tetany, weakness, seizures and ECG changes; correct under local protocol.

Nursing care and monitoring

Measure urine output accurately, including hourly output when unstable, and document fluid balance and daily weight.
Monitor BP, ECG, RR, SpO₂, mental state, temperature, oedema, rash and lung sounds.
Check medicine doses, renal clearance, interactions and timing; record any suspected adverse reaction.
Maintain aseptic catheter care, skin protection, nutrition and safe mobility.
Escalate fever, rash with hypotension, oliguria, hyperkalaemia, breathlessness, confusion, seizure or chest pain.
Explain investigations, biopsy, dialysis possibility and follow-up using teach-back.

Complications

Complication	Clues	Response
AKI/hyperkalaemia	Oliguria, weakness, ECG changes or rising creatinine.	Emergency renal/electrolyte pathway and nephrology review.
Fluid overload	Crackles, hypoxia, orthopnoea, oedema and hypertension.	Upright, oxygen/ventilation, fluid review and diuresis/dialysis assessment.
Severe electrolyte wasting	Weakness, cramps, arrhythmia, tetany or seizures.	ECG, urgent replacement and repeat levels.
Sepsis/immune disease	Fever, hypotension, rash, joint/lung symptoms or shock.	Cultures, antibiotics/source control and specialist therapy.
Chronic kidney disease	Persistent creatinine, anaemia, hypertension or proteinuria.	Nephrology follow-up, renal protection and long-term education.

Prevention and discharge

Record drug allergies and suspected nephrotoxic reactions clearly; advise the patient to report them everywhere.
Avoid unsupervised NSAIDs, herbal mixtures and over-the-counter medicines during kidney illness.
Maintain appropriate hydration, especially during fever, diarrhoea or heat exposure, unless fluid restricted.
Repeat renal function/electrolytes after discharge and review medicine doses.
Teach return precautions: reduced urine, swelling, breathlessness, fever/rash, palpitations, severe weakness or confusion.

Clinical scenarios

Scenario 1 – Drug-induced ATIN: A patient develops fever, rash, eosinophilia and rising creatinine two weeks after an antibiotic. Stop the suspected medicine under senior direction, assess sepsis and renal complications, and arrange urgent nephrology review.

Scenario 2 – Tubular injury after shock: A patient recovering from septic shock becomes oliguric with acidosis. Monitor ECG/electrolytes, maintain euvolaemia, avoid nephrotoxins and discuss renal replacement if complications persist.

Scenario 3 – Chronic tubulointerstitial disease: A patient has years of nocturia, polyuria, bland urine and slowly declining eGFR. Arrange renal evaluation, medication/toxin review, electrolyte testing and CKD education.

Common errors to avoid

Waiting for fever, rash and eosinophilia before considering ATIN.
Continuing the suspected medicine while awaiting biopsy.
Giving large fluids to an overloaded patient or withholding fluids from true shock.
Ignoring electrolyte wasting, polyuria or acid-base disturbance.
Failing to review herbal remedies, occupational exposures and over-the-counter medicines.
Discharging without repeat renal tests and specialist follow-up.

TUBULE SAFE: T – Timeline medicines/exposures; U – Urine and output; B – BP/breathing; U – Urgent electrolytes; L – Look for systemic disease; E – Escalate renal failure. S – Stop culprit; A – Assess volume; F – Follow labs; E – Educate.

Revision questions

What is the difference between glomerular and tubulointerstitial disease?
List common medicine causes of acute interstitial nephritis.
Why can the classic fever-rash-eosinophilia triad be absent?
What tests assess tubular function and dangerous complications?
When should steroids or renal replacement be considered?
How do chronic tubulointerstitial diseases present?
Write a nursing plan for a patient with ATIN and oliguria.

Key takeaways

Acute tubulointerstitial disease is often reversible when the trigger is removed early.
Medication reconciliation and urine/creatinine trends are central to diagnosis.
Manage sepsis, shock, obstruction, electrolyte disorders and fluid overload promptly.
Do not delay nephrology referral in AKI, systemic disease or suspected ATIN.
Clear documentation of drug reactions prevents future kidney injury.

References for further study

Tubulointerstitial Diseases: Recognition, Assessment and Emergency Management Read More »

Kidney Stones and Renal Colic: Emergency Assessment and Management

Why this topic matters: Kidney stones can cause severe renal colic, vomiting, haematuria and urinary obstruction. Most small uncomplicated stones pass, but an infected obstructed kidney, solitary kidney obstruction, bilateral obstruction, anuria, uncontrolled pain or acute kidney injury can become life-threatening. EMT students must separate uncomplicated colic from sepsis, ectopic pregnancy, abdominal catastrophe and obstructive uropathy requiring urgent decompression.

Learning objectives

Explain stone formation, movement and the typical pattern of renal colic.
Recognise red flags for infected obstruction, AKI, anuria and alternative emergencies.
Perform focused history, examination, urine testing, blood tests and appropriate imaging.
Describe analgesia, antiemetics, fluids, antibiotics, urology referral and definitive treatment.
Provide prevention, stone analysis, dietary advice and follow-up education.

Definition and pathophysiology

Kidney stones are crystalline deposits formed when urine becomes supersaturated with substances such as calcium, oxalate, phosphate, uric acid or cystine. A stone may remain in the kidney without symptoms or move into the ureter. Stretching and spasm of the ureter produce colicky pain; obstruction increases upstream pressure and can impair renal function. A stone plus infection is a dangerous combination because bacteria may be trapped behind the obstruction.

Stone risk is increased by low urine volume, heat and dehydration, high salt intake, metabolic disorders, recurrent urinary infection, family history, obesity, certain medicines and anatomical abnormalities.

Typical presentation

Feature	Typical pattern	Important caution
Pain	Sudden severe flank/back pain radiating to groin or genital area; patient may be unable to keep still.	Constant pain, peritonism or pain out of proportion needs alternative diagnosis.
Urinary symptoms	Frequency, urgency, dysuria or inability to pass urine when stone is distal.	Fever/dysuria may indicate infected obstruction.
Haematuria	Pink, red, brown or microscopic blood.	Absence of haematuria does not exclude a stone; visible blood has other serious causes.
Gastrointestinal symptoms	Nausea, vomiting, sweating and restlessness.	Persistent vomiting causes dehydration and AKI.
Infection signs	Fever, rigors, chills, tachycardia, hypotension or confusion.	Obstructed infected kidney is a urological emergency.

Red flags requiring urgent escalation

Fever, rigors, sepsis, immunosuppression or a toxic appearance.
Anuria, very low urine output, rising creatinine or hyperkalaemia.
Solitary kidney, renal transplant, bilateral obstruction or known CKD.
Uncontrolled pain or vomiting despite treatment.
Pregnancy, child, older frail patient or diagnostic uncertainty.
Peritonism, pulsatile abdominal mass, syncope, vaginal bleeding, testicular pain or suspected ectopic pregnancy.

Triage and first contact

Assess ABCDE, pain score, temperature, pulse, BP, hydration, urine output and sepsis signs.
Ask onset, radiation, previous stones, fever, dysuria, urine output, pregnancy possibility, medications and renal history.
Check for abdominal, vascular, gynaecological, testicular and spinal alternatives.
Establish IV access for severe pain/vomiting or instability; collect urine and blood tests early.
Pre-alert urology for suspected infected obstruction or anuria; do not discharge while awaiting deterioration.

Focused examination

Observe restlessness, pallor, sweating, dehydration, fever and toxic appearance.
Check flank/CVA tenderness, abdominal tenderness, guarding, rigidity, bowel sounds and pulsatile mass.
Assess genital/testicular findings when indicated and perform pregnancy assessment in reproductive-age patients.
Check lungs and heart for fluid status, sepsis or alternative cardiopulmonary disease.
Record urine output and inspect for catheter obstruction or retention.

Investigations

Investigation	Purpose	Clinical point
Urine dipstick/microscopy and culture	Detect blood, leucocytes, nitrites, protein and infection.	Culture suspected infection; pyuria with obstruction is high risk.
FBC, CRP, renal profile/electrolytes	Assess infection, AKI, dehydration and metabolic complications.	Rising creatinine or potassium requires urgent renal/urology input.
Pregnancy test	Guide imaging and differential diagnosis.	Consider ectopic pregnancy and use ultrasound when pregnant.
Ultrasound	Detect hydronephrosis, obstruction, bladder retention and pregnancy-safe findings.	First-line in pregnancy and commonly in children.
Low-dose non-contrast CT	Confirm stone size/location and alternative diagnosis in adults.	Use urgent local pathway; do not delay treatment of sepsis or shock.
Stone analysis/metabolic urine studies	Identify recurrence risk and prevention plan.	Arrange after acute episode through urology/renal follow-up.

Analgesia and symptom control

Use the local renal-colic protocol. NSAIDs are often first-line when renal function, hydration, bleeding risk, allergy, pregnancy and gastrointestinal status permit.
Use paracetamol or prescribed opioid analgesia when NSAIDs are contraindicated or inadequate; monitor sedation and breathing.
Give antiemetics for vomiting and reassess hydration and electrolyte status.
Avoid giving large volumes of fluid simply to “force” a stone through; replace dehydration carefully and monitor obstruction/overload.
Document pain score before and after treatment, dose, route, response and adverse effects.

Infected obstructed kidney

Fever or sepsis with a blocked ureter is an emergency. Antibiotics alone may not sterilise an obstructed system. Treat sepsis immediately, obtain cultures where feasible and arrange urgent drainage by ureteric stent or nephrostomy under urology.

ABCDE, sepsis assessment, oxygen for hypoxaemia and IV access.
Blood/urine cultures without delaying broad-spectrum antibiotics according to local protocol.
Carefully reassessed fluids, lactate/urine monitoring and vasopressors in critical care when shock persists.
Urgent imaging and urology consultation for decompression; definitive stone removal usually waits until infection is controlled.
Monitor for AKI, hyperkalaemia, respiratory failure and septic shock.

Definitive treatment and referral

Small stones likely to pass may receive observation, analgesia, antiemetics and selected medical expulsive therapy under urology guidance.
Ureteroscopy, shock-wave lithotripsy or percutaneous nephrolithotomy may be used according to size, location, obstruction, infection and local resources.
Persistent intolerable pain, unlikely passage, obstruction, infection, impaired renal function or a solitary kidney need urgent specialist decision.
Collect a passed stone when possible for composition analysis; recurrence prevention depends on stone type and metabolic risk.

Nursing interventions and monitoring

Record pain, vital signs, temperature, urine output, nausea/vomiting, hydration and response to every medicine.
Strain urine only when requested and preserve a passed stone safely for analysis.
Maintain IV access, reassess lungs after fluids and monitor renal function/electrolytes.
Observe for fever, rigors, hypotension, confusion, anuria or worsening pain and escalate immediately.
Prepare patients for imaging, stent/nephrostomy, lithotripsy or surgery; provide privacy and clear explanations.
Teach hydration and medication instructions without encouraging unsafe overhydration during obstruction.

Prevention and lifestyle

Maintain adequate fluid intake across the day, especially in hot climates, unless a clinician has prescribed fluid restriction.
Reduce excessive salt and follow stone-specific dietary advice; do not eliminate dietary calcium without specialist advice.
Moderate animal protein and high-oxalate foods when indicated by stone analysis.
Manage obesity, gout, hyperparathyroidism, recurrent infection and bowel disease.
Review medicines that increase stone risk and arrange metabolic evaluation for recurrent, bilateral, childhood or complicated stones.

Complications

Complication	Clues	Response
Infected obstruction	Fever, pyuria, rigors, hypotension or confusion.	Sepsis care, antibiotics and urgent drainage.
Acute kidney injury	Oliguria, anuria, rising creatinine or potassium.	Renal profile, ECG and urgent urology/renal review.
Hydronephrosis	Persistent obstruction, flank pain or ultrasound dilation.	Urology referral and decompression decision.
Medication toxicity	GI bleeding, bronchospasm, AKI, sedation or hypotension.	Stop/review medicines and treat adverse effects.
Misdiagnosis	Peritonism, vascular collapse, ectopic pregnancy or testicular torsion.	Broaden differential and activate the relevant emergency pathway.

Clinical scenarios

Scenario 1 – Uncomplicated colic: A stable adult has flank-to-groin pain, microscopic haematuria, no fever and normal renal function. Treat pain/nausea, arrange appropriate imaging and follow-up, and provide strict return precautions.

Scenario 2 – Infected obstruction: A patient with a known ureteric stone has fever, rigors, tachycardia and reduced urine. Start sepsis care and antibiotics, obtain cultures, and arrange urgent urological decompression.

Scenario 3 – Pregnancy: A pregnant patient has severe flank pain and vomiting. Assess maternal stability, urine and infection, use ultrasound first and involve obstetric/urology teams.

Common errors to avoid

Discharging a febrile patient with an obstructed stone after analgesia alone.
Giving excessive IV fluids to force stone passage.
Using NSAIDs without checking AKI, dehydration, pregnancy, bleeding or allergy risk.
Ignoring anuria, solitary kidney or rising creatinine.
Assuming every flank pain is renal colic without considering ectopic pregnancy, AAA, appendicitis, torsion or pyelonephritis.
Failing to provide return precautions and stone-prevention follow-up.

STONE SAFE: S – Sepsis and shock; T – Time pain/onset; O – Output and obstruction; N – NSAID safety; E – Examine alternatives. S – Scan appropriately; A – Analgesia/antiemetic; F – Follow-up; E – Escalate infected obstruction.

Revision questions

Why is an infected obstructed kidney a urological emergency?
Describe typical renal-colic pain and list important alternative diagnoses.
What tests are required in a patient with suspected renal colic?
When are ultrasound and non-contrast CT preferred?
What factors make NSAIDs unsafe?
What signs require urgent urology/renal referral?
Write discharge teaching for recurrent kidney stones.

Key takeaways

Most uncomplicated small stones pass, but infection plus obstruction is life-threatening.
Assess sepsis, renal function, urine output, pregnancy and alternative emergencies.
Give effective analgesia and antiemetics while arranging appropriate imaging.
Do not delay antibiotics or decompression in infected obstruction.
Prevention requires stone analysis, hydration and personalised metabolic advice.

References for further study

Kidney Stones and Renal Colic: Emergency Assessment and Management Read More »