Transcript DO NO HARM
…. a headache! Salma Naheed Jeffrey Luna Mfon Ewang The History Mrs. K.S. 53 y.o. Morrocan Female PC 20/10/03: Vomiting Fever SOB + Cough Headaches Abdominal Pain HPC Vomiting: - early morning - ×5 - no blood Abdominal Pain: - 5 day history - sharp, paroxysmal pain - lower abdomen - radiates to RUQ - worse in early morning - v.severe Cough: - white sputum - °haemoptysis Headaches: - early morning - in temporal region - severe - dizziness PMH 10/96: - adenocarcinoma of R upper lobe - R thoracotomy + R upper lobectomy 04/02: Palliative radiotherapy: whole brain irradiation delivering 20 Gy in 5 fractions 02/03: - steroid-induced diabetes 09/03: - in Morocco: diabetic ketoacidotic coma 03/02: brain 2° in L frontal region + R occipital region 04/02: - Hypertension DH Regular Prescriptions - Mixtard 30 10 units manes 8 units nocte - Lansoprazole 30 mg - Frusemide 80mg - Dexamethasone 500mcg - Bisoprolol 10mg - Nystatin 1 ml - Paracetamol 1g - Coamoxiclav 1.2g - Erythromycin 500mg - Senna Prn Medications: - Cyclisine 50mg - Codeine Phosphate 30mg - Glycerine Suppositories - Oromorph 2.5-5.0mg No known allergies FH 85 Old age 53 25 4 SH Married with 1 daughter Formerly a cleaner in A+E at St. Georges Lives in a flat with her husband Life-long non-smoker (husband does smoke) Tea-total SE CVS - NAD RESP: - dysuria - °haemoptysis GI: - lost weight: July 86kg > Oct 63kg - diminished appetite - constipation (last opened bowels 3 days ago) CNS: - poor vision - ° paraesthesia - cough + SOB GU: LMS: - NAD The Examination O/E Unwell lady Temp 37.5°C °JACCOL oral thrush CVS HR = 64 beats/min Pulse regular BP = 119/64 JVP HS: I-II-O °murmur Resp RR = 21/min R sided thoracotomy scar Trachea central bronchial breath sounds on L upper zone of L lung R lung: vesicular breathing xxxx xxxx GI generalised tenderness more tender on RUQ °guarding °rebound tenderness °organomegaly °palpable masses BS - present PR - not done XXX ×××× XXX Cranial Nerve Examination Visual acuity v.poor unable to assess CNII,III,IV+VI CNV,VII-XII normal Examination of Limbs UL LL Tone Power R N 5/5 L N 5/5 R N 5/5 L N 5/5 Sensation: - Light touch - JPS Reflexes ++ ++ ++ ++ ++ ++ ++ ++ ++ ++ The Investigations Investigations 20/10/03 Na K Cl Bic Ur Glu Bil 139 3.6 112 22 8.9 9.2 19 Alt ALP Alb Hb WBC CRP 35 281 28 12.9 29.4 374.6 CXR (21/10/03) Chest AP: - R hemidiaphragm raised - extensive air space change throughout L lung - L heart border obscured - v.likely infective process affecting L upper lobe Abdominal USS (23/10/03) Multiple lesions throughout liver (3×3cm) mass on R adrenal gland (metastases?) 3.5cm fluid density lesion on lower pole of L kidney (represents parapelvic cyst) R kidney, gallbladder, spleen + pancreas unremarkable CT Scan (head) 23/10/03 2 separate lesions: - R frontal lobe - L post. parietal region R frontal area - ass. with oedema midline shift to R + dilatation of L temporal horn Impression Raised ICP? Consolidation? Incomplete Bowel Obstruction? Hypercalcaemia? Summary 53 y.o. female with a history of metastatic adenocarcinoma of the R lung who presented with malaise probably due to raised ICP + consolidation of left lung. Brain Metastases A brief overview Brain Metastases Most common type of brain tumour in adults develop in ~10-30% of adults with cancer 1/3rd-1/4th develop as single tumour, multiple mets. are more common nature of primary cancer is related to # of brain mets. and may affect response to treatment Sources of Brain Mets. May result from any 1° tumour, most commonly: lung breast unknown melanoma colon breast, 50% 15-20% 10-15% 10% 5% colon, renal cell mets. - usu. single melanoma, lung mets. - usu. multiple Spread & Distribution Most commonly spread is haematogenous deposits often found at junction of grey and white matter high density of blood vessels vessels decrease in size, trapping emboli also common in ‘watershed’ areas distribution follows relative weight and blood flow for each area: 80% are in cerebral hemispheres 15% in cerebellum 5% in brainstem Signs & Symptoms > 2/3rds of patients with cerebral mets. will experience neurologic symptoms clinical features vary new neurologic symptoms in any cancer patient may indicate developing brain mets. problems may result from: ‘Mass effect’ increased intracranial pressure tumour growth swelling due to excess fluid (oedema) blockage of CSF irritation/destruction of brain cells Signs & Symptoms 2 Common features associated with brain mets.: Focal neurological dysfunction (PC in 20-40%) Behavioural/cognitive dysfunction (PC in 35%) Seizures (PC in 10-20%) Headache Muscle weakness Raised intracranial pressure causing: Papilloedema Confusion Nausea & vomiting Stroke due to: Embolization of tumour cells Tumour invasion/compression of an artery Diagnosis Brain mets. produce similar features to those of many other conditions image chest & abdomen if no known primary brain mets. can be distinguished from 1° brain tumours and other lesions by imaging gadolinium-enhanced MRI is primary imaging choice; CT also used exact diagnosis requires tissue biopsy Brain Met. Characteristics usu. solid, spherical well-defined margins soft center filled with dead cells zone of active tumour cells that appear as a ringlike structure on scan widespread oedema multiple lesions common usu. localized at grey-white matter junction Treatment Options Symptomatic Management Corticosteroids Anticonvulsants Definitive Treatment Surgery Radiotherapy Chemotherapy Symptomatic 1 Corticosteroids Corticosteroids help relieve symptoms of mass effect by dexamethasone - the standard treatment for peritumoural oedema since 1961 reducing leakage from damaged vessel linings reducing CSF production increasing cerebral blood flow low mineralocorticoid activity (vs. other corticosteroids) symptomatic improvement within 24-72h in most patients side effects: myopathy, wt. gain, hyperglycaemia, insomnia, gastritis, immunosuppresion, etc. must reduce dose gradually with improvement or following radiotherapy Symptomatic Meds. 2 Anticonvulsants for e.g. phenytoin those with a history/complaint of seizures little use as prophylaxis can interact w/other drugs inc. steroids and common chemotherapeutic drugs Definitive Treatment: Surgery Tumour resection recommended for lesions that are: solitary met. accessible, esp. if > 3cm diameter symptomatic w/evidence of mass effect not radiosensitive In patients with: Karnofsky > 70 life expectancy > 3 months Surgery 2 resection of single met. often followed by Whole Brain Radiotherapy (WBRT) Example: -single lesion -surgically accessible -diameter > 3cm -good KPS surgery + WBRT Radiotherapy 65-85% of patients respond on average reduces neurologic symptoms and has palliative effect often used in combination with surgery, chemotherapy and symptomatic meds. effectiveness depends on tumour histology radioresistant: radiosensitive: melanoma, renal cell Ca lymphoma, SCC lung Radiotherapy 2 Earlier treatment generally provides better outcome WBRT is the most common treatment for cerebral metastases since most patients present with multiple mets. for single mets. surgery + WBRT appears to provide longer survival longer length of functional independence than surgery alone. Whole Brain Radiation Side effects Acute: transient worsening of neuro. effects nausea, vomiting, hair loss, otitis Delayed: neuro. symptoms from radiation necrosis more frequently with high dose per fraction - dementia, ataxia - leukoencephalopathy Chemotherapy Generally poor results for treatment of brain mets., possibly due to: chemo. agent chosen for ability to penetrate BBB may not be most effective vs. 1° Ca intrinsic chemoresistance of Ca’s that spread to brain brain mets. often develop after primary agents have failed to control systemic disease some success vs. mets. from chemosensitive tumours. e.g. breast Ca, SCC lung, germ cell Ca Treatment Results / Prognosis Treatment None Medical (steroids, anticonvulsants) Med + WBRT Med + surgery + WBRT Median Survival 1 month 2 months w/limited extracranial disease 10-16 months 4-6 months 10-12 months Summary Overall prognosis is poor because of extracranial disease; majority do not die from brain mets. since effective palliation is available single lesions in relatively healthy patients should be considered for surgery followed by RT; multiple lesions for WBRT controversy wrt. treatment remains, research ongoing STEROID-INDUCED DIABETES MELLITUS BY MFON EWANG DIABETES MELLITUS Hyperglycaemic state Diagnostic criteria (American diabetes association) Symptoms of diabetes + plasma glucose concentration >11.1mmol/L at anytime & without regards to meal Fasting plasma glucose >7mmol/L Plasma glucose concentration >11.1mmol/L 2hr after 75g of oral glucose IDDM NIDDM Early onset Late onset Polyuria Overweight Polydipsia Twin studies show Weight loss 90% concordance Fatigue and malaise Obesity Features of ketoacidosis Twin studies show 1015% concordance Viruses and dietary factors Immunological factors Poor foetal development Other types of diabetes mellitus Gestational diabetes mellitus Endocrinopathies assoc Acromegaly Cushing’s syndrome Phaeochromocytoma Drug induced DM Drug-induced DM Interfere with insulin production and secretion β cell death (pentamidine) Inhibits insulin secretion (β-antagonist, diphenylhydantoin) Act on insulin secretion and sensitivity insulin sensitivity (Thiazides) Inhibits islet cell function & insulin resistance (Cyclosporin A & Tacrolimus) nutrient flux (nicotinic acid) Steroid-induced DM ↓effectiveness of insulin in regulating metabolism Glucocorticoids (Hydrocortisone, Dexamethasone, prednisolone) Organ transplants, Asthma, malignancies, rheumatological syn., skin disorders etc. Actual incidence of DM induced unknown Pathophysiology of steroid induced DM Glucocorticoids encourage breakdown of stored proteins and fat stores Induce cellular concentrations of gluconeogenic enzymes 1 &2 = hepatic glucose output Effect of insulin diminished in the presence of steroids Glucocorticoids induce PPAR- ? peripheral gluc. Uptake due to insulin resistance and direct steroid effects Management Treatment for steroid induced DM similar to NIDDM Supportive treatment Education Diet Oral control hypoglycaemics Sulphonylureas, Insulin Metformin (mandatory in type 1) Management Chromium picolinate Corticosteroid Voglibose Delays treatment chromium loss (-glucosidase inhibitor) glucose absorption steroid dose or stop Complications Macrovascular Atherosclerosis Artheromatous lesion predisposes to MI, peripheral vascular disease, or stroke Microvascular Retinopathy Nephropathy Neuropathy Conclusion Steroid are commonly used medications, which can induce DM Presentation same as with any other type Polydipsia, polyuria, weight loss etc. Management similar to type 2 -glucosidase inhibitor & Chromium picolinate (recommended)