Category Archives: Malawi medicine

A 19 year old albino with a skin lesion

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A 19 year old lady from Blantyre, Malawi, attends with a scaly lesion which has been present on her right cheek for 3 months.

  1. Can you describe what you see?
  2. What is the diagnosis?
  3. What is your management?

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This is an albino woman with a small (approx 1 cm) superficial looking red scaly lesion on her right lateral cheek.  She has some lentigines (the brown marks) and coarse wrinkled neck skin.  If palpated the skin over the red lesion feels rough.

This is an actinic keratosis (actinic/solar – sunlight (UV) induced, keratosis – scaly/horny growth).  Considered to be pre-malignant, actinic keratoses are most often seen in exposed skin in fair skinned individuals who have had excessive UV light.

An actinic keratosis may follow 1 of 3 paths: it may regress, it may persist unchanged, or it may progress to invasive squamous cell carcinoma. The actual percentage that progress to invasive squamous cell carcinoma remains unknown, and estimates have varied from as low as 0.1% to as high as 10%.  Generally, thicker lesions are more likely to progress.

She should be advised to avoid further damaging sun exposure by wearing a wide-brimmed hat, clothing which covers the skin and a high factor sunscreen on exposed sites.  The actinic keratosis can be treated in several ways including medical management with creams and surgical management.  As she has several further actinic keratoses on her neck and other cheek (not seen in the photo above) and as other treatment modalities are not available in the clinic she is treated with imiquimod.  This is an expensive treatment, but had been donated to the clinic from an overseas organisation.

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A man with a foot ulcer

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A 42 year old man attends the dermatology clinic in Queen Elizabeth Central Hospital, Blantyre in 2012 with an ulcer on the sole of his right foot.  He says that it has been present since 2004 but that he underwent surgery 1 and a half years ago.  He was told it was a squamous cell carcinoma.  It initially healed, but since then the skin has broken down and the ulcer is enlarging in size.  He went back to see the surgeons and they have sent him on to dermatology to get dressings.

  1. Can you describe what you see?
  2. What diagnoses would you consider? Is there any information that would be ideal to have that would help point you towards the most likely diagnosis?
  3. Would you like to examine any other part of his body?
  4. What would you do next?

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This is a deep, irregulary shaped ulcer on the mid-sole of the right foot.  There is no cm scale in the photo, but it must be at least 5 cm in diameter.  The ulcer looks relatively clean.  The base of the ulcer comprises of  red fleshy tissue.  It is not possible to see bone or tendons.

In this case the most likely explanation is recurrence of squamous cell carcinoma (SCC). It would be helpful to get his pathology report from his operation 18 months ago to confirm that it was SCC and to see whether it was completely excised at the time.

The differential diagnoses includes a neuropathic ulcer (this is less likely as the ulcer does not correspond to the area of sole with maximal pressure, and he has no history of neuropathy) and infection (which in this geographical setting may include fungi and mycobacteria: but note there is little discharge, swelling or surrounding inflammation).

You would want to examine his ipsilateral inguinal and femoral lymph nodes to check for signs of metastasis and if they are palpable a fine needle aspirate (or lymph node biopsy) should be sent to pathology.

A biopsy of the base of the ulcer for pathology would confirm or refute the diagnosis of recurrence of SCC.

A surgical opinion as to whether this is operable should be sought.

This case was contributed by Levie Mwale and Ann Sergeant

An unwell lady with a history of breast cancer

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A 53 year old female presents to the Queen Elizabeth Hospital, Blantyre with a 2 day history of drowsiness, diarrhoea and vomiting.

Her past medical history includes hypertension, diabetes and recently diagnosed breast cancer.

On examination she is dehydrated, BP 95/60, pulse 120/min, temp 380C, O2 sats 90% on air and Glasgow Coma Score of 14/15 (E4V4M6).

  1. What other history is required?
  2. What diagnoses would you consider?
  3. What immediate tests are indicated?
  4. What treatment would you start?


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Is she on chemotherapy for her breast cancer? If so you would worry about the possibility of neutropenic sepsis.  Immediate tests would include a blood sugar level (quick to do and vital in anyone with a history drowsiness – and we know she has diabetes), urgent full blood count (FBC) and blood cultures.  Less urgent tests include a chest X ray, urine dipstick (send for microscopy and culture if indicated) and urea and electrolytes.

Intravenous (IV) fluids,  IV broad spectrum antibiotics and oxygen should be started as soon as possible.

FBC results: Hb 66, WCC 0.8, Plt 34.

This case was contributed by Ewan Brown and Leo Masamba.

 



A 4 year old boy with patchy hair loss

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A healthy 4 year old boy is brought to the Dermatology clinic at Queen Elizabeth Central Hospital, Blantyre by his parents.  He has been scratching his head, and they have recently noticed that he has developed several small scaly areas with associated hair loss.

What is your diagnosis and how would you treat him?

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The diagnosis is tinea capitis (scalp “ringworm”).  This is a cutaneous fungal infection which invades the hair shaft and is often due to Trichophyton tonsurans (caught from other children) or Microsporum canis (caught from kittens or puppies). Without treatment it gets better spontaneously at puberty.  After puberty it only occurs in patients with underlying immunosuppression.

Treatment of choice is oral griseofulvin 15-20mg/kg/day for 6 weeks.  Additional application of a topical antifungal, during the early stages of treatment, may reduce the risk of transmission.  Terbinafine is an unlicensed alternative, but may not be as effective for infections with M. canis.   The only oral antifungal available in the department is ketoconazole, so he is prescribed this and topical Whitfield’s ointment.  His parents then tell you that his elder sister was treated with the same treatment successfully earlier this year.

Other siblings with infection should also be treated and if the family pet’s fur is falling out it must be treated too.

The other differential diagnosis to consider in this case is alopecia areata but the presence of scale distinguishes these diagnoses.

Further info

 

This case contributed by Levie Mwale and Ann Sergeant

 

A 22 year old man with a painful rash

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A 22 year old plumber attends the drop-in clinic in the dermatology department at Queen Elizabeth Central Hospital, Blantyre.  He has a 1 day history of a painful vesicular rash on his right buttock and posterior thigh. He feels unwell with fever.

Right posterior thigh

  1. What is your diagnosis?
  2. What is your management?

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This is herpes zoster infection also known as “shingles”.  Varicella zoster virus (VZV) lies dormant in the posterior root ganglion after chicken pox.  Reactivation causes the virus to travel down the cutaneous nerves to infect epidermal cells in the skin.    The presence of pain and the dermatomal distribution is classical.  As the rash is less than 72 hours old it is worthwhile treating with antiviral medication such as aciclovir, famciclovir or valaciclovir, if available.  They inhibit VZV replication and reduce the severity and duration of the rash.  Postherpetic neuralgia (pain which persists >3months after the rash has resolved) is more common in elderly patients and may respond to tricyclic antidepressant drugs, which should be started early if possible.

He is treated with aciclovir 800mg 5 times daily for 7 days and regular paracetemol.

In a young man in an HIV prevalent region, underlying HIV should be suspected (Herpes zoster is categorised by the World Health Organisation as clinical stage 2 of HIV infection) and an HIV test performed.

His HIV test was positive.  His CD4 count should be checked and if ≤350 cells/mm3 antiretroviral therapy commenced.

Further info

This case contributed by Levie Mwale and Ann Sergeant

A 34 year-old man with a fit

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A 34 year old man presents to Queen Elizabeth Central Hospital, Blantyre with a 2 day history of frontal headaches and generalized tonic clonic seizures. His guardians report that he has had multiple nodules all over his body since childhood but has previously been well.

He has another prolonged seizure after admission. He is post-ictal on examination with a Glasgow Coma Scale 11/15 (E -4, V-2, M-5). His pupils are of normal size and equally reacting to light. His vital signs on admission are: blood pressure 121/81mmHg, pulse 94/min, temperature  37.0°C, respiratory rate 24/min. The chest and abdominal examination are normal. The rest of the neurological exam does not reveal  any focal deficits.

  1. What is his underlying condition?
  2. What differential diagnoses are you considering?
  3. What tests would you want to do?
  4. What would your initial management be?

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The recent history of headaches raises the possibility that this is more than simple epilepsy, though his underlying condition is associated with epilepsy.  This is a region where there is a high prevalence of HIV infection, the possibility of which broadens the differential diagnosis importantly.

His underlying condition is  neurofibromatosis type 1.  It is associated with epilepsy and with astrocytomas, gliomas, but at presentation it may be causative or just a coincidence.  

Tests you should seek:

  • Blood glucose
  • Full blood count
  • Malaria blood film
  • Lumbar puncture with examination to include India Ink stain (if available you would test for Cryptococcal antigen)
  • HIV test
  • Urea and electrolytes
  • Brain imaging (but CT /MRI not available here)
  • Serology for syphilis

Differential diagnosis

  • Epilepsy – simple or caused by neurofibromatosis-associated brain lesions
  • Cerebral malaria is more likely in children than adults
  • Metabolic – DEFG; Don’t ever forget Glucose.  Hypoglycaemia may induce coma and convulsions.  Other metabolic disturbances including hyponatraemia
  • Meningitis – particularly TB or Cryptococcal meningitis in the presence of HIV infection
  • Infective focal brain lesions:  Toxoplasmosis, primary CNS lymphoma – usually HIV-related; Cysticercosis, neurosyphilis

Initial management

  • Control continuing convulsions with diazepam IV.

Then in this setting:

  • Phenobarbitone 600mg loading dose (infusion or slow push) the 90mg maintenance (IM or orally if patient can tolerate it) OR Phenytoin 900mg loading dose (infusion) then 100mg tds maintenance.  Blood monitoring is not available.
  • Empirical cover for meningitis until CSF results back: Ceftriaxone 2g bd IV

For options in other centres, see …

This case contributed by Dr Tamara Phiri

 

A 16 year old girl with oedema

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A 16 year old girl presents to Queen Elizabeth Hospital, Blantyre with a two-month history of facial oedema.  It is worse in the morning, slightly better at night and not associated with shortness of breath or cough.  She has been well recently, with no intercurrent illnesses. Some kind of antimicrobial was prescribed a month ago, but the swelling was present then and has increased since.

On examination she is slim but has marked bilateral pitting pedal oedema and facial puffiness; her abdomen is also distended, with shifting dullness.  She is apyrexial.  General examination is unremarkable.  Her BP is 112/65, pulse 72.  She has reduced breath sounds and dullness to percussion at both lung bases.  Heart sounds and abdomen are normal and she has no neurological deficit.

A urine dipstick shows 4+ protein.  She has a serum creatinine of 60 micromol/l (0.7 mg/dl) and a normal blood count.  Tests of liver function, serum proteins are not available.

  1. What is the differential diagnosis?
  2. Renal biopsy is not immediately available here.  What management will you recommend?  How will you advise her and her parents?

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With 4+ proteinuria and oedema there can be little doubt that she has nephrotic syndrome.  It is ‘pure’ nephrotic syndrome, meaning heavy proteinuria without any haematuria, which puts it at the extreme left hand end of the spectrum (see Glomerulonephritis) and makes it significantly less likely that it is caused by post-streptococcal glomerulonephritis or other disorder more toward the ‘nephritic’ end of the spectrum.

She should severely restrict salt intake: oedema is caused by salt retention.  Diuretics are often required, usually loop diuretics.

HIV is an important condition in this region.  An HIV test is important both because the condition could be a manifestion of HIV affecting the kidney, and because most active treatments for nephrotic syndrome involve immunosuppressive agents.

Minimal change disease would be the most likely explanation in a Caucasian girl.  However FSGS is more common as a cause of nephrotic syndrome in Africans: one of these two conditions is most likely. SLE is very unusual before menarche.

If she is HIV negative, a trial of prednisolone, 1mg/kg/day for a few weeks would be worthwhile.

Further info

This case is was contributed by Fran Th’ng and Gavin Dreyer

A 25 year old woman with a rash and raised creatinine

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A 25 year old woman is referred with a 6 month history of fatigue, joint pain, pleuritic chest pain and facial rash. Three months ago at another hospital she was found to be unwell with a Creatinine of 500 micromol/l, Hb 8.2 g/dl, and urinalysis showed 3+ protein, 3+ blood. She was treated with some tablets (identity unknown) and a subsequent creatinine was 200 and Hb rose to 12 g/dl. Now she is unwell again.

On examination she has a rash around her nose and on her cheeks. She is febrile, 38.2C, and has mild swelling of her left and right MCPJ. She is slim and does not look Cushingoid. BP 155/87. There is no oedema and examination of chest, cardiovascular system and abdomen are normal. She has a platelet count of 50 and Hb 6.2g/dl, Creatinine 430 micromol/l, and urinalysis continues to show 3+ for both protein and blood.

Three questions:

  1. What is the likely underlying diagnosis?
  2. What other urgent (not too complicated) test results are important?
  3. How would you treat the underlying disease given that a renal  biopsy is not possible?

Thanks to Dr Gavin Dreyer for this case.

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Diagnosis:  Lupus seems the most likely underlying diagnosis.

Tests (1) She had a high level of Malaria falciparum parasitaemia. (2) She was HIV non-reactive.
Neither infection would do well with immunosuppressive therapy for lupus. The level of HIV positivity in the region is high, but in sick patients, in particular medical inpatients, it is much higher (up to 80%).
Ideal initial treatment according to WHO should be Artemisinin combination therapy, but it is not generally affordable so Quinine is still most commonly used. She responded to treatment and her Hb rose.

Treatment beyond this point is difficult, but almost certainly she has aggressive inflammatory disease in view of the creatinine changes, and will need cyclophosphamide. Some might argue for MMF in a young woman, but it is less well tested, and much more expensive.

Other diagnostic possibilities?
Classic HIV nephropathy usually has a more extreme nephrotic phase. Of course many other renal pathologies can occur in HIV infection.

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An HIV positive woman with low eGFR

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A 38 year old woman who has been on anti-retroviral therapy for 3 years is found to have a creatinine of 230 micromol/l (2.6 mg/dl).  She is taking Tenofivir, Efavirenz and cotrimoxazole and has been compliant with therapy.  She complains of recurrent dysuria and frequency, as well as intermittent fevers which do not always seem related to urinary symptoms.  She describes some vaginal discharge.

On examination she is thin but not emaciated.  She has no oedema.  Her pulse is 64, blood pressure 110/60, chest is clear, cardiovascular system normal.  She has mild non-specific abdominal tenderness but no masses.

Urine dipstick is positive for nitrites and leucocytes, blood 1+.

What type of disease process do you suspect?  What further features or investigations would you immediately seek?

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She has marked renal impairment; that creatinine corresponds to an eGFR of about 26.  She already has possible explanations for renal disease from her diagnosis of HIV and the fact that she is on anti-HIV drugs, many of which have renal side effects, including crystallization, interstitial nephritis, tubular injury.

A key observation is the bland urinary sediment, showing little protein or blood, which essentially rules out severe glomerular pathology.  HIV nephropathy is a glomerulopathy, so it is an unlikely explanation. Using the pre-renal/renal/post-renal algorithm, this makes you home in on

  • Pre-renal causes.  She doesn’t sound very dehydrated, but pre-renal causes include arterial and small vessel disease; for instance thrombotic microangiopathy can occur in HIV.
  • Interstitial or tubular causes (drugs particularly likely to be implicated; tenofivir is associated with tubular injury)
  • Obstruction

The key investigation in any patient with renal failure and urinary symptoms is renal imaging.  Ultrasound is quick, non-invasive, risk-free, and almost always first choice; it should be part of the investigation of almost any patient with unexplained new severe CKD.  It showed bilateral hydroureter and hydronephrosis without distention of the bladder.

Hope you had also written that vaginal examination is one of the things that you must do here.  She had advanced cervical cancer involving both ureters.

She also had a CD4 count of 93 despite her anti-HIV therapy, with PCR showing 5,000 copies per ml, suggesting anti-retroviral failure.  In a well-resourced setting you would consider testing for drug resistance.

Further info

Thanks to Fran Th’ng and Gavin Dreyer for this case.

Renal failure from the HIV clinic

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A 32 year old man presents wtih 3 days of vomiting, nausea, and malaise.  HIV was diagnosed 6 months ago but he has not been started on ant-retroviral therapy.  He has no other significant past medical history.

He is apyrexial.  BP is 100/60 and pulse 82.  He has no oedema.  JVP is not visible when lying flat.

Urine dipstick shows 1+ protein only.  The only other investigation available is serum creatinine – 700 micromol/l (8 mg/dl).

What do you think are the main diagnostic possibilities here?  What additional key questions would you like to ask? What would your initial management be?

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(To follow!)

Case contributed by Fran Th’Ng and Gavin Dreyer