52.INGLES #1 (5 INTENTOS)

A 15-YEAR-OLD BOY WAS BROUGHT TO CASUALTY BY HIS PARENTS. HE HAD BEEN FEBRILE AND GENERALLY UNWELL FOR 2 DAYS, BUT ON THE DAY OF
PRESENTATION HAD SPIKED A HIGH FEVER, BECOME SLIGHTLY CONFUSED AND STARTED VOMITING. A CT HEAD SCAN WAS UNREMARKABLE AND A
LUMBAR PUNCTURE WAS PERFORMED. A GRAM STAIN OF HIS CEREBROSPINAL FLUID IS SHOWN. WHAT IS THE DIAGNOSIS?

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A 46-YEAR-OLD MAN WAS ADMITTED TO CASUALTY FROM HOME WITH A ONE WEEK HISTORY OF MILD GLOBAL HEADACHE. ON THE DAY OF ADMISSION HE FOUND DIFFICULTY IN EXPRESSING HIMSELF VERBALLY. HE HAD A GENERALISED SEIZURE IN THE AMBULANCE ON THE WAY TO HOSPITAL. ON EXAMINATION HE WAS FULLY CONSCIOUS WITH A GLASGOW COMA SCALE SCORE OF 15/15. HE WAS FEBRILE (380 C) WITH PULSE 80 BEATS PER MINUTE IN SINUS RHYTHM AND BLOOD PRESSURE 130/75 MMHG. THERE WAS NO NUCHAL RIGIDITY. NEUROLOGICAL EXAMINATION REVEALED AN EXPRESSIVE DYSPHASIA AND MILD RIGHT SIDED WEAKNESS. AN MRI SCAN OF HIS BRAIN SHOWED ABNORMAL SIGNALS IN BOTH TEMPORAL LOBES, BUT WAS MOST PROMINENT ON THE LEFT WHERE A DEGREE OF MASS EFFECT WAS NOTED. A LUMBAR PUNCTURE WAS PERFORMED AND CSF ANALYSIS SHOWED: OPENING PRESSURE: NORMAL CSF PROTEIN: NORMAL CSF GLUCOSE: NOMAL CELLS: 9 LYMPHOCYTES/MM3 GRAM STAIN: NEGATIVE. WHAT IS THE MOST LIKELY DIAGNOSIS?
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A 63-YEAR-OLD MAN WAS ADMITTED TO HOSPITAL WITH ACUTE ONSET OF SEVERE CHEST PAIN. HE HAD A HISTORY OF HYPERTENSION AND HYPERCHOLESTEROLAEMIA, WITH NO PREVIOUS HISTORY OF ISCHAEMIC HEART DISEASE. HIS ELECTROCARDIOGRAM SHOWED INFERIOR ST SEGMENT ELEVATION AND HE WAS THROMBOLYSED IN THE CARDIAC CARE UNIT. HE MADE A GOOD RECOVERY, BUT THREE DAYS LATER BECAME ACUTELY BREATHLESS. ON EXAMINATION HE HAD A RESPIRATORY RATE OF 36 PER MINUTE AND A PULSE OF 128 BEATS PER MINUTE AND REGULAR. HIS BLOOD PRESSURE WAS 80/45MMHG AND OXYGEN SATURATIONS WERE 85% ON ROOM AIR. AUSCULTATION REVEALED A GALLOP RHYTHM AND A HARSH SYSTOLIC MURMUR AT THE APEX. CHEST EXAMINATION REVEALED WIDESPREAD CRACKLES AND WHEEZES. HIS CHEST RADIOGRAPHY IS SHOWN BELOW:
WHAT IS THE MOST LIKELY EXPLANATION FOR THESE FINDINGS?

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A 33-YEAR-OLD FEMALE PRESENTS WITH A ONE YEAR HISTORY OF GALACTORRHOEA AND AMENORRHOEA. SHE INFORMS YOU THAT SHE DOES NOT WANT TO BECOME PREGNANT. ON EXAMINATION THERE IS GALACTORRHOEA TO EXPRESSION AND VISUAL FIELDS ARE NORMAL TO CONFRONTATION.INVESTIGATIONS CONFIRM THE DIAGNOSIS OF A MACROPROLACTINOMA, WITH A PROLACTIN CONCENTRATION OF 10,500 MU/L (50-500) AND MRI OF THE PITUITARY REVEALING A 1.5 CM TUMOUR WITH SOME SUPRASELLAR EXTENSION. WHAT IS THE MOST APPROPRIATE TREATMENT FOR THIS WOMAN?
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A 28-YEAR-OLD EXECUTIVE IS REFERRED BECAUSE HE HAS BEEN DRINKING EXCESSIVELY OVER THE PAST TWO WEEKS. HE REPORTS FEELING “DOWN” FOR ABOUT A MONTH, CRYING FREQUENTLY AND HAVING NO INTEREST IN SEX OR WORK. HE ADMITS TO HAVING HAD SIMILAR DOWN PERIODS IN THE LAST 10 YEARS. HOWEVER, HE ALSO DESCRIBES HIMSELF HAVING PERIODS OF ELATION DURING WHICH HE IS GREGARIOUS, PRODUCTIVE AND OPTIMISTIC. DURING THESE TIMES, HE SAYS THAT HE DOES NOT DRINK AT ALL. WHAT IS THE MOST LIKELY DIAGNOSIS? (PLEASE SELECT AN OPTION)
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YOU ARE ASKED TO SEE A 40 YEAR-OLD WOMAN COMPLAINING OF “EMOTIONAL TURMOIL”. SHE GIVES A TEN MONTH HISTORY OF PERIODS OF INTENSE ANXIETY AND FEAR, ASSOCIATED WITH PALPITATIONS, TREMULOUSNESS, SWEATING AND A FEELING OF SUFFOCATION. SHE DOES NOT GIVE ANY CLEAR ANTECEDENT EVENT SETTING OFF HER SYMPTOMS. THESE EPISODES, WHICH NORMALLY LAST 10-15 MINUTES, OCCUR IN A VARIETY OF SETTINGS, INCLUDING WHEN SHE IS RELAXED. HOWEVER, THEY ARE MOST LIKELY TO OCCUR WHEN SHE IS RIDING ON AN ESCALATOR. SHE HAS NO PSYCHOTIC SYMPTOMS. SHE HAS TWICE RUSHED TO THE ACCIDENT AND EMERGENCY DEPARTMENT THINKING THAT SHE WAS HAVING A HEART ATTACK, BUT TESTS WERE NORMAL EACH TIME. SHE HAD SIMILAR EPISODES 5 YEARS EARLIER, WHICH GRADUALLY SUBSIDED. HER MOTHER SUFFERED FROM DEPRESSION AND HER FATHER DIED AT THE AGE OF 45 YEARS WITH A MYOCARDIAL INFARCTION. HER GENERAL PHYSICAL HEALTH WAS GOOD. SHE WAS ALERT AND ORIENTATED. APART FROM MILD IMPAIRMENT OF CONCENTRATION, HER COGNITIVE FUNCTIONS WERE INTACT. WHAT IS THE MOST LIKELY DIAGNOSIS WITH THE DATA PRESENTED? (PLEASE SELECT AN OPTION)
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A 21-YEAR-OLD FEMALE WITH A FOUR YEAR HISTORY OF TYPE 1 DIABETES IS ADMITTED WITH DYSURIA, FEVER AND RIGORS. SHE HAS BEEN USING MIXED INSULIN TWICE DAILY AND HER LAST HBA1C WAS 7.2% AT ANNUAL REVIEW THREE MONTHS AGO. ON EXAMINATION, SHE HAS A TEMPERATURE OF390. A BLOOD PRESSURE OF 112/76 MMHG AND A PULSE OF 110 BPM. CARDIOVASCULAR AND RESPIRATORY EXAMINATION ARE UNREMARKABLE. SHE HAS DIFFUSE TENDERNESS ON ABDOMINAL EXAMINATION. RESULTS ON ADMISSION SHOW: PLASMA GLUCOSE 640MG/DL PH 7.1 (7.35-7.45) STANDARD BICARBONATE 9MMOL/L (22-28) THE PATIENT IS COMMENCED ON IV SLIDING SCALE INSULIN. WHICH OF THE FOLLOWING IS THE MOST APPROPRIATE MANAGEMENT STRATEGY OF HER PH STATUS?
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A 45-YEAR-OLD LADY IS REFERRED TO THE OUTPATIENT CLINIC BY HER GENERAL PRACTITIONER FOLLOWING THE FINDING OF SIGNIFICANT HYPERTENSION ON A ROUTINE CHECK-UP. HER BLOOD PRESSURE IN CLINIC IS MEASURED AT 180/100 MMHG. HER ELECTROCARDIOGRAM REVEALS CHANGES CHARACTERISTIC OF LEFT VENTRICULAR HYPERTROPHY. WHAT IS THE MOST LIKELY CAUSE FOR HER HYPERTENSION? (PLEASE SELECT AN OPTION)
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A 70-YEAR-OLD MAN COMPLAINS OF PAIN IN THE CHEST OVER THE LAST THREE MONTHS ASSOCIATED WITH A 7KG WEIGHT LOSS. HE IS A SMOKER OF 10 CIGARETTES DAILY. AFTER INITIAL CHEST X-RAYS A CT SCAN WAS PERFORMED. WHAT IS THE DIAGNOSIS?

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A 30-YEAR-OLD WOMEN AT 33 WEEKS GESTATION WAS REVIEWED IN AN ANTE-NATAL CLINIC. SHE IS KNOWN TO HAVE DIABETIC RENAL DISEASE AND HAS BEEN COMPLAINING OF INCREASING ANKLE OEDEMA, HEADACHES AND BLURRED VISION FOR THE LAST 24 HOURS. IN ADDITION, SHE VOMITED TWICE THIS MORNING AFTER BREAKFAST AND IS NOW FEELING NAUSEAS. HER BLOOD PRESSURE IN CLINIC WAS ELEVATED AT 170 SYSTOLIC AND 100 DIASTOLIC AND SHE WAS ADMITTED TO LABOUR WARD FOR TREATMENT OF PRE-ECLAMPSIA. SHE WAS STARTED ON A MAGNESIUM SULPHATE INFUSION FOR TREATMENT OF PRE-ECLAMPSIA. DURING THE INFUSION, SHE COMPLAINED OF FACIAL FLUSHING, WORSENING NAUSEA AND BLURRED VISION BUT HER HEADACHES WERE STARTING TO IMPROVE. HER BLOOD PRESSURE WAS ALSO NOTED TO BE FALLING TO 105 SYSTOLIC AND 70 DIASTOLIC. A MIDWIFE FOLLOWING A CHANGE IN SHIFT HAD NOTED THE PATIENT WAS SLURRING HER SPEECH AND THE PATIENT WAS COMPLAINING OF DOUBLE VISION. HOWEVER, THE PATIENT HAD THOUGHT THIS WAS PROBABLY DUE TO FATIGUE. SEVERAL HOURS LATER, THE MIDWIFE FOUND THE PATIENT TO BE BARELY ROUSABLE WITH A BRADYCARDIA OF 55 BEATS PER MINUTE. WHAT IS THE MOST LIKELY CAUSE OF HER SYMPTOMS? (PLEASE SELECT AN OPTION)
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62-YEAR-OLD MAN WAS REFERRED BY HIS GENERAL PRACTITIONER FOR AN OUTPATIENT ENDOSCOPY. THE PATIENT GAVE A FOUR- WEEK HISTORY OF WORSENING ODYNOPHAGIA AND DYSPHAGIA. HE ATTRIBUTED THE ONSET OF HIS SYMPTOMS TO A COURSE OF ANTIBIOTICS THAT HE RECEIVED FROM HIS GP FOR A SORE THROAT SIX WEEKS PREVIOUSLY. HE HAD NO PAST MEDICAL HISTORY OF NOTE. INVESTIGATIONS PERFORMED BY HIS GP REVEALED: HAEMOGLOBIN 9.1 G/DL (13.0-18.0) MCV 94 FL (80-96) WHITE CELL COUNT 2.79 X109/L (4-11 X109) NEUTROPHILS 1.2 X109/L (1.5-7 X109) LYMPHOCYTES 0.8 X109/L (1.5-4 X109) MONOCYTES 0.7 X109/L (0-0.8 X109) EOSINOPHILS 0.04 X109/L (0.04-0.4 X109) BASOPHILS 0.05 X109/L (0-0.1 X109)
PLATELETS 124 X109/L (150-400 X109). UPPER GASTROINTESTINAL ENDOSCOPY DEMONSTRATED EXTENSIVE OESOPHAGEAL CANDIDIASIS. WHAT TREATMENT, IF ANY, IS REQUIRED?
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A 69-YEAR-OLD MAN WAS ADMITTED TO HOSPITAL WITH A THREE-WEEK HISTORY OF INCREASING EXERTIONAL DYSPNOEA. THERE WAS NO HISTORY OF COUGH OR SPUTUM PRODUCTION, BUT HE COMPLAINED OF SWEATS AT NIGHT. HE GAVE A TWO-MONTH HISTORY OF GENERAL MALAISE AND ANOREXIA AND REPORTED WEIGHT LOSS OF APPROXIMATELY 8KG. THERE WAS NO OTHER PAST HISTORY OF NOTE. HE DID NOT TAKE ANY REGULAR MEDICATIONS. ON EXAMINATION HE APPEARED PALE. HIS TEMPERATURE WAS 37.5°C. TWO FINGER NAIL-FOLD INFARCTS WERE NOTED AND A SMALL SPLINTER HAEMORRHAGE IN HIS LEFT GREAT TOE. HIS PULSE WAS 100 BEATS PER MINUTE AND REGULAR WITH A BLOOD PRESSURE OF 110/75 MMHG. HIS HEART SOUNDS WERE NORMAL WITH A PANSYSTOLIC MURMUR HEARD LOUDEST AT THE APEX AND RADIATING TO THE AXILLA. NO DIASTOLIC MURMUR WAS HEARD. HIS CHEST WAS CLEAR. THE ABDOMEN WAS SOFT AND SLIGHTLY TENDER IN THE LEFT UPPER QUADRANT WHERE THE TIP OF THE SPLEEN COULD BE PALPATED 3CM BELOW THE LEFT COSTAL MATGIN. INVESTIGATIONS SHOWED: HAEMOGLOBIN 9.8 G/DL (13.0-
18.0) MCV 92 FL (80-96) WHITE BLOOD CELLS 7.9 X109/L (4-11 X109) PLATELETS 102 X109/L (150-400 X109) ESR 110 MM/1STHOUR (0-20) SERUM SODIUM 138 MMOL/L (137-144) SERUM POTASSIUM 4.1 MMOL/L (3.5-4.9) SERUM UREA 8.1 MMOL/L (25-7.5) SERUM CREATININE 150 ΜMOL/L(60-110) URINALYSIS BLOOD ++ . BLOOD CULTURES STREPTOCOCCUS BOVIS GROWN IN ALL BOTTLES A TRANSTHORACIC ECHOCARDIOGRAM SHOWED TWO VEGETATIONS ON THE MITRAL VALVE LEAFLETS. THE PATIENT WAS STARTED ON APPROPRIATE ANTIBIOTIC THERAPY. WHAT ADDITIONAL INVESTIGATION SHOULD BE PERFORMED?
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A PREVIOUSLY WELL 46 YEAR-OLD MAN PRESENTS WITH A TWO DAY HISTORY OF PROGRESSIVELY WORSENING HEADACHES,
DIZZINESS, DOUBLE VISION, DRY MOUTH AND SWALLOWING DIFFICULTIES. HIS WIFE HAS ALSO NOTICED THAT HIS FACE HAS BEEN
SLIGHTLY ASYMMETRICAL OVER THE LAST DAY OR SO. HE DENIES ANY SENSORY OR GASTROINTESTINAL SYMPTOMS. THREE DAYS
AGO HE INJURED HIS LEFT HAND WHILE GARDENING AND THE WOUND ON HIS LITTLE FINGER IS RED AND TENDER. ON EXAMINATION
HE IS ALERT AND ORIENTATED. PULSE IS 60 BEATS/MIN, BP 130/65 MMHG, TEMPERATURE 38OC. HE HAS PTOSIS, LARGE
POORLY REACTIVE PUPILS, DIPLOPIA ON LOOKING TO THE EXTREMITIES HORIZONTALLY BILATERALLY, WEAKNESS OF CLOSING THE
EYELIDS (RIGHT WORSE THAN LEFT) AND INABILITY TO WHISTLE PROPERLY. HE ALSO CHOKES WHEN ASKED TO SWALLOW A LITTLE
WATER. POWER IS MILDLY GENERALLY REDUCED IN THE UPPER LIMBS AND LOWER LIMBS. DEEP TENDON REFLEXES ARE GENERALLY
DEPRESSED AND SENSATION IS NORMAL. INVESTIGATIONS REVEAL: HAEMOGLOBIN 14.0 G/DL (13.0-18.0) WHITE BLOOD COUNT
10.0 X109/L (4-11 X109) PLATELETS 200 X109/L (150-400 X109) SERUM SODIUM 139 MMOL/L (137-144) SERUM
POTASSIUM 4.0 MMOL/L (3.5-4.9) SERUM UREA 6.8 MMOL/L (2.5-7.5) PLASMA GLUCOSE 7.5 MMOL/L (3.0-6.0) CSF
EXAMINATION OPENING PRESSURE 15 MM H20 (50-180) CELL COUNT < 2 PER MM3 CSF PROTEIN 0.3 G/L (0.15-0.45) CSF
GLUCOSE 6.1 MMOL/L (3.3-4.4) WHAT IS THE MOST LIKELY DIAGNOSIS?
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A 46 YEAR-OLD MAN IS ADMITTED FEELING GENERALLY UNWELL. HE COMPLAINS OF INCREASING STIFFNESS IN HIS ARMS AND JAWS. HE HAS A MILD THROBBING FRONTAL HEADACHE WHICH HE SAYS IS TYPICAL OF MIGRAINE FROM WHICH HE IS KNOWN TO SUFFER FROM. HE ALSO HAS A HISTORY OF SCHIZOPHRENIA AND LAST VISITED THE PSYCHIATRIST A MONTH AGO. MEDICATIONS INCLUDE SUMATRIPTAN AND FLUPHENAZINE, BOTH OF WHICH HE HAS BEEN ON FOR APPROXIMATELY TWO YEARS. ON EXAMINATION, HIS PULSE IS 90 BEATS/MIN, BP 180/85 MMHG AND TEMPERATURE 38.50C. PULSATILE TEMPORAL ARTERIES ARE NOTED BILATERALLY. NEUROLOGICAL EXAMINATION REVEALS MILD GENERALIZED INCREASE IN TONE THROUGHOUT BUT IS OTHERWISE UNREMARKABLE. INVESTIGATIONS: HB 12.6 G/DL (13.0-18.0) WCC 4.9 X109/L (4-11 X109) PLATELETS 200 X109/L (150-400 X109) ESR 5 MM/HR (0-15) PLASMA SODIUM 145 MMOL/L (137-144) PLASMA POTASSIUM 3.7 MMOL/L (3.5-4.9) PLASMA UREA 4.9 MMOL/L (2.5-7.5) WHICH OF THE FOLLOWING DRUG TREATMENTS WOULD YOU CONSIDER FOR THIS PATIENT’S CONDITION?
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A 68 YEAR-OLD LADY PRESENTS TO THE CASUALTY DEPARTMENT WITH INCREASING BREATHLESSNESS AND COUGHING UP OF SMALL AMOUNTS OF BLOOD OVER THE PAST ONE WEEK. SHE ALSO COMPLAINS OF FREQUENT NOSEBLEEDS AND HEADACHES OVER THE PAST TWO MONTHS. SHE FEELS GENERALLY LETHARGIC AND HAS LOST A STONE IN WEIGHT. ON EXAMINATION, SHE HAS NO CYANOSIS, FINGER CLUBBING, PALLOR OR A SKIN RASH. PULSE IS 100 BEATS/MIN AND BP 135/95. RESPIRATORY RATE IS 28 BREATHS/MIN, CHEST EXPANSION MODERATE AND ON AUSCULTATION THERE IS INSPIRATORY CRACKLES AT THE LEFT LUNG BASE. INVESTIGATIONS: HB 10.0 G/DL (11.5-16.5) WCC 19.9 X109/L (4-11 X109) PLATELETS 540 X109/L (150-400 X109) PLASMA SODIUM 139 MMOL/L (137-144) PLASMA POTASSIUM 5.3 MMOL/L (3.5-4.9) PLASMA UREA 30.6 MMOL/L (2.5-7.5) PLASMA
CREATININE 760 UMOL/L (60-110) PLASMA GLUCOSE 5.8 MMOL/L (3.0-6.0) PLASMA BICARBONATE 8 MMOL/L (20-28) PLASMA CALCIUM 2.23 MMOL/L (2.2-2.6) PLASMA PHOSPHATE 1.7 MMOL/L (0.8-1.4) PLASMA ALBUMIN 33 G/L (37-49) BILIRUBIN 8 ΜΠ。VL (1-22) PLASMA ALKALINE PHOSPHATASE 380 U/L (45-105 >14 YEARS) PLASMA ASPARTATE TRANSAMINASE 65 U/L (1 31) ARTERIAL BLOOD GASES ON AIR PH 7.2 (7.36-7.44) PCO2 4.0 KPA (4.7-6.0) PO2 9.5 KPA (11.3-12.6) ECG SINUS TACHYCARDIA CHEST X-RAY SHADOW IN LEFT LOWER LOBE URINALYSIS BLOOD PROTEIN ++ WHICH IS THE BEST DESCRIPTIVE ACID-BASE ABNORMALITY OF THIS PATIENT?
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A 69 YEAR-OLD LADY PRESENTS TO YOU COMPLAINING OF BEING NON-SPECIFICALLY UNWELL OVER THE LAST MONTH. SHE I STIFF ESPECIALLY IN THE MORNINGS AND HAS DIFFICULTY LIFTING HER HANDS TO COMB HER HAIR. HER ARMS AND SHOULDERS ACHE CONSTANTLY AND SHE HAS JAW PAIN WHEN CHEWING. SHE HAS LOST 4KG IN WEIGHT AND HAS A PERSISTENT HEADACHE. SHE SMOKES 10 CIGARETTES A DAY AND CONSUMES 10 UNITS OF ALCOHOL A WEEK. ON EXAMINATION, TEMPERATURE IS 380C, PULSE 84 BEATS/MIN AND BP 125/80. THE EXAMINATION IS OTHERWISE UNREMARKABLE. INVESTIGATIONS: HB 9.9 G/DL (11.5-16.5) WCC 13.9X109/L (4-11 X109) PLATELETS 400 X109/L (150-400 X109) PLASMA SODIUM 139 MMOL/L (137-144).
PLASMA POTASSIUM 4.7 MMOL/L (3.5-4.9) PLASMA UREA 5.0 MMOL/L (2.5-7.5) PLASMA CREATININE 109 ΜMOL/L (60-110)
PLASMA GLUCOSE 5.9 MMOL/L (3.0-6.0) BILIRUBIN 15 UMOL/L (1-22) PLASMA ALKALINE PHOSPHATASE 390 U/L (45-105)
PLASMA ASPARTATE TRANSAMINASE 65 U/L (1-31) PLASMA CREATINE KINASE 150 U/L (24-170) WHAT IS THE MOST APPROPRIATE INVESTIGATION TO BE PERFORMED NEXT?
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A 40 YEAR-OLD LABOURER IS REFERRED TO YOU WITH COMPLAINTS OF PAIN AND SWELLING IN BOTH HANDS OVER THE LAST SIX MONTHS. THE JOINTS ARE MOST STIFF IN THE MORNINGS. HE TAKES DICLOFENAC TABLETS WHICH RELIEVE THE PAIN. HIS WORK INVOLVES THE USE OF VIBRATING TOOLS. EXAMINATION REVEALS THAT THE METACARPOPHALANGEAL JOINTS AND WRISTS OF BOTH HANDS ARE WARM, SWOLLEN AND TENDER.
INVESTIGATIONS:
HB 9.8 G/DL (13.0-18.0)
WCC 7.9 X109/L (4-11 X109)
PLATELETS 430 X109/L (150-400 X109)
ESR 68 MM/HR (0-15)
PLASMA SODIUM 141 MMOL/L (137-144)
PLASMA POTASSIUM 4.1 MMOL/L (3.5-4.9)
PLASMA UREA 5.9 MMOL/L (2.5-7.5)
PLASMA CREATININE 105 ΜMOL/L (60-110)
PLASMA GLUCOSE 4.8 MMOL/L (3.0-6.0)
X-RAY OF HANDS PERIARTICULAR DECALCIFICATION
WHAT IS THE MOST LIKELY DIAGNOSIS?
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A 42-YEAR-OLD WIDOW PRESENTS WITH A ONE WEEK HISTORY OF PROGRESSIVE CONFUSION AND UNSTEADY GAIT. SHE WORKS AS A BARMAID AND LIVES IN POOR SOCIAL CIRCUMSTANCES. ON EXAMINATION SHE IS MALNOURISHED AND DISORIENTATED. SHE HAS NYSTAGMUS AND IS UNABLE TO ABDUCT EITHER EYE. THE PUPILS ARE SLUGGISH AND UNEQUAL. ANKLE JERKS ARE ABSENT BUT UPPER LIMB REFLEXES ARE PRESENT. SHORTLY AFTER HER ADMISSION YOU ARE CALLED TO THE WARD AS SHE HAS BECOME VERY DROWSY AND HAS COLLAPSED ON THE FLOOR. INVESTIGATIONS ON ADMISSION SHOWED: HAEMOGLOBIN 11.4 G/DL (11.5- 16.5) MCV 99 FL (80-96) WHITE BLOOD CELLS 5.6 X109/L (4-11 X109) PLATELETS 230 X109/L (150-400 X109) SERUM SODIUM 129 MMOL/L (137-144) SERUM POTASSIUM 3.2 MMOL/L (3.5-4.9) SERUM BILIRUBIN 27 UMOL/L (1-22) SERUM GAMMA GLUTAMYL TRANSFERASE 440 U/L (4-35) SERUM ALKALINE PHOSPHATASE 180 U/L (45-105) SERUM ASPARTATE AMINOTRANSFERASE 90 U/L (1-31) SERUM ALANINE AMINOTRANSFERASE 45 U/L (5-35) SERUM ALBUMIN 33 G/L (37-49)
PROTHROMBIN TIME 12 SECS (11.5-15.5) THE FIRST INVESTIGATION SHOULD BE:
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A 42-YEAR-OLD WIDOW PRESENTS WITH A ONE WEEK HISTORY OF PROGRESSIVE CONFUSION AND UNSTEADY GAIT. SHE WORKS AS A BARMAID AND LIVES IN POOR SOCIAL CIRCUMSTANCES. ON EXAMINATION SHE IS MALNOURISHED AND DISORIENTATED. SHE HAS NYSTAGMUS AND IS UNABLE TO ABDUCT EITHER EYE. THE PUPILS ARE SLUGGISH AND UNEQUAL. ANKLE JERKS ARE ABSENT BUT UPPER LIMB REFLEXES ARE PRESENT. SHORTLY AFTER HER ADMISSION YOU ARE CALLED TO THE WARD AS SHE HAS BECOME VERY DROWSY AND HAS COLLAPSED ON THE FLOOR. INVESTIGATIONS ON ADMISSION WERE AS FOLLOWS: HAEMOGLOBIN 11.4 G/DL (11.5-16.5) MCV 99 FL (80-96) WHITE BLOOD COUNT 5.6 X109/L (4-11 X109) PLATELETS 230 X109/L (150-400 X109) SERUM SODIUM 129 MMOL/L (137-144) SERUM POTASSIUM 3.2 MMOL/L (3.5-4.9) SERUM BILIRUBIN 27 ΜMOL/L (1-22) SERUM
GAMMA GT 440 U/L (4-35) SERUM ALKALINE PHOSPHATASE 180U/L (45-105) SERUM AST 90 U/L (1-31) SERUM ALT 45 U/L (5-35) SERUM ALBUMIN 33 G/L (37-49) PROTHROMBIN TIME 12 SECS (11.5-15.5) WHAT WAS IS THE MOST LIKELY CAUSE OF HER PRESENTATION AND DROWSINESS?
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A 50-YEAR-OLD WOMAN PRESENTS WITH 6 MONTHS HISTORY OF PROGRESSIVE PROBLEMS WITH HER GAIT AND RECURRENT FALLS. SHE IS KNOWN TO HAVE HYPOTHYROIDISM AND INSULIN DEPENDENT DIABETES. SHE IS A NON-SMOKER, DRINKS 10 UNITS OF ALCOHOL EVER WEEK. SHE IS ON THYROXINE AND INSULIN. THERE IS A FAMILY HISTORY OF DIABETES AND HYPERTHYROIDISM. ON EXAMINATION, SHE HAS A BROAD BASE GAIT. SHE NEEDS TO LOOK DOWN TO THE FLOOR WHEN SHE WALKS. SHE HAS A POSITIVE ROMBERG’S TEST. CRANIAL NERVE EXAMINATION IS NORMAL. EXAMINATION OF THE UPPER IS NORMAL. SHE HAS INCREASED TONE IN LOWER LIMBS WITH BILATERAL EXTENSOR PLANTAR RESPONSE. BOTH KNEE AND ANKLE REFLEXES ARE ABSENT. PAIN AND TEMPERATURE SENSATION IS NORMAL. VIBRATION WAS REDUCED UP TO THE KNEES AND JOINT POSITION WAS ABSENT DISTALLY. THERE ARE NO WASTING OR FASCICULATIONS. GENERAL MEDICAL EXAMINATION IS NORMAL. MRI BRAIN AND WHOLE SPINE IS NORMAL. WHAT IS THE MOST LIKELY DIAGNOSIS?
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A 19 YEAR-OLD-GIRL WAS FOUND BY HER FATHER SEMI-CONSCIOUS IN HER BEDROOM. SHE WAS SURROUNDED BY EMPTY PACKETS OF HIS MEDICATION WHICH CONSISTED OF DIGOXIN AND ASPIRIN. THERE WAS ALSO EVIDENCE THAT SHE MAY HAVE CO- INGESTED A LARGE AMOUNT OF ALCOHOL. SHE WAS LAST SEEN 8 HOURS PREVIOUSLY AND HER FATHER ESTIMATED THAT SHE COULD HAVE TAKEN THE TABLETS AT ANYTIME SINCE THEN. ON ARRIVAL TO HOSPITAL SHE HAD A GLASGOW COMA SCORE OF 13/15, A PULSE RATE OF 40 BEATS PER MINUTE, BLOOD PRESSURE 80MMHG SYSTOLIC AND 50 MMHG DIASTOLIC. A 12-LEAD ECG SHOWED A BRADYCARDIA OF 38 BEATS PER MINUTE WITH A 2:1 HEART BLOCK. INVESTIGATIONS SHOWED: SERUM SODIUM 140 MMOL/L (137-144) SERUM POTASSIUM 5.9 MMOL/L (3.5-4.9) SERUM CHLORIDE 98 MMOL/L (100-108) SERUM BICARBONATE 20 MMOL/L (20-30) SERUM UREA 9.2 MMOL/L (25-75) SERUM CREATININE 130 ΜMOL/L (60-110) PLASMA GLUCOSE 5.2 MMOL/L (3.0-6.0) DIGOXIN LEVEL 8 NMOL/L (THERAPEUTIC RANGE 1-2 NMOL/L) SALICYLATE LEVEL <10MG/DL FULL BLOOD COUNT AND ARTERIAL BLOOD GASES WERE NORMAL. SHE HAD A GOOD INITIAL RESPONSE WITH INTRAVENOUS ATROPINE, WHICH TRANSIENTLY INCREASED HER HEART RATE TO 60 BEATS PER MINUTE BUT HER BLOOD PRESSURE REMAINED LOW AT 〈90MMHG SYSTOLIC. SHORTLY AFTER THE INTRAVENOUS ATROPINE SHE STARTED HAVING INTERMITTENT EPISODES OF BROAD COMPLEX TACHYCARDIA. WHICH WOULD BE THE MOST APPROPRIATE TREATMENT FOR THIS PATIENT? (PLEASE SELECT AN OPTION)
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A 38 YEAR-OLD MAN PRESENTS WITH AN EPISODE OF RIGHT-SIDED WEAKNESS AFFECTING HIS RIGHT ARM AND LEG. THE WEAKNESS OCCURRED WHILE HE WAS EATING BREAKFAST AND RESOLVED COMPLETELY IN 30 MINUTES. THREE MONTHS EARLIER HE HAS AN EPISODE OF SLURRED SPEECH LASTING A FEW MINUTES AND HAD BEING INVESTIGATED EXTENSIVELY IN HOSPITAL ASPIRIN 75 MG HAD BEEN STARTED AS TREATMENT. ON EXAMINATION, HE IS OVERWEIGHT WITH A BMI OF 38, PULSE 88 BEATS/MIN REGULAR AND BP 140/85 MMHG. HEART SOUNDS ARE NORMAL AND NO CAROTID BRUITS ARE DETECTABLE. THE NEUROLOGICAL EXAMINATION IS UNREMARKABLE EXCEPT FOR AN UPGOING PLANTAR RESPONSE ON THE RIGHT SIDE.. A DOPPLER ULTRASOUND OF THE CAROTID ARTERIES REVEAL 50% STENOSIS IN THE PROXIMAL CAROTID ARTERIES BILATERALLY. WHAT EVIDENCE- BASED INTERVENTION IS MOST LIKELY TO PREVENT FURTHER EPISODES OF THE PATIENT’S CONDITION?
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WHAT IS THE DIAGNOSIS IN THIS PATIENT WITH RECURRENT ANEMIA? BASED ON THE IMAGE. SELECT AN OPTION:
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A 54-YEAR-OLD MALE DIABETIC WITH A FIVE YEAR HISTORY OF TYPE 2 DIABETES PRESENTS AT ANNUAL REVIEW. HE IS CURRENTLY RECEIVING GLIBENCLAMIDE 5 MG DAILY, TOGETHER WITH LISINOPRIL 10 MG DAILY FOR HYPERTENSION. ON EXAMINATION HE HAS A BMI OF 32.4 KG/M2, A BLOOD PRESSURE OF 132/84 MMHG, ALL PULSES ARE PALPABLE AND HE HAS SOME LOSS OF VIBRATION SENSATION ON BOTH BIG TOES AND HAS 2 TO 3 DOT HAEMORRHAGES IN EACH EYE. INVESTIGATIONS REVEAL. HB1AC 10.2% (3.8-64), TOTAL CHOLESTEROL 5.2 MMOL/L (<5.2), TRIGLYCERIDES 2.2 MMOL/L (0.45-1.69), URINALYSIS: NEGATIVE. WHAT IS THE MOST APPROPRIATE TREATMENT FOR THIS PATIENT’S HYPERGLYCAEMIA?
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A 74-YEAR-OLD FEMALE PRESENTS AS AN ACUTE ADMISSION WITH CONFUSION AND DIARRHOEA. LITTLE IS KNOWN OF HER PAST MEDICAL HISTORY EXCEPT THAT IT IS NOTED ON THE GP LETTER THAT SHE IS RECEIVING TREATMENT FOR MANIC DEPRESSION AND HYPOTHYROIDISM. EXAMINATION REVEALS THAT SHE HAS A GLASGOW COMA SCALE OF 15 BUT IS CONFUSED. SHE IS THIN, UNKEMPT AND DEHYDRATED WITH A TEMPERATURE OF 37OC. SHE HAS A PULSE OF 82 BEATS PER MINUTE IN A REGULAR RHYTHM AND A BLOOD PRESSURE OF 112/72 MMHG. SHE IS NOTED TO HAVE A COARSE TREMOR AND DYSARTHRIC SPEECH. WHICH OF THE FOLLOWING IS THE MOST APPROPRIATE INVESTIGATION TO ASSIST IN HER MANAGEMENT?
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A 16-YEAR-OLD MALE PRESENTED TO HOSPITAL WITH A 24 HOUR HISTORY OF FEVER AND CONFUSION. HE WAS KNOWN TO HAVE EPILEPSY, WHICH WAS WELL CONTROLLED ON DRUGS. HE ALSO HAD A PREVIOUS HISTORY OF DRUG OVERDOSE. HE CONSUMED 50 UNITS OF ALCOHOL PER WEEK AND ADMITTED TO USING RECREATIONAL DRUGS. ON EXAMINATION HIS TEMPERATURE WAS 39OC. INVESTIGATIONS: HAEMOGLOBIN 11 G/DL (13.0-18.0), WHITE CELL COUNT 11 X109/L (4-11 X109), PLATELETS 156 X109/L (150-400 X109), SERUM SODIUM 127 MMOL/L (137-144), SERUM POTASSIUM 4.1 MMOL/L (3.5-4.9), SERUM UREA 12 MMOL/L (2.5-7.5), SERUM CREATININE 160 UMOL/L (60-110), SERUM ALT 300 U/L (5-35), SERUM AST 250 U/L (1-31), SERUM ALP 120 U/L (45-105), SERUM BILIRUBIN 20 ΜMOL/L (1-22), SERUM GGT 400 U/L (<50), URINE PROTEIN +. HIS CHEST X-RAY ON ADMISSION IS SHOWN. WHAT IS THE BEST COMBINATION OF ANTIBIOTICS IN THE FIRST INSTANCE?

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A 69-YEAR-OLD MAN PRESENTED TO HIS GP WITH A FOUR-MONTH HISTORY OF WEAKNESS OF HIS LOWER LIMBS. HE HAD NOTICED SOME DIFFICULTY WALKING UP AND DOWN STAIRS AND MORE RECENTLY HAD NOTICED A CONSTANT DRY MOUTH AND MILD DROOPING OF HIS EYELIDS. HE DENIED ANY PROBLEMS WITH SWALLOWING OR ANY VISUAL DISTURBANCES AND HAD NOT NOTICED ANY CHANGE IN SENSATION IN HIS LEGS, OR ALTERATION IN BLADDER FUNCTION. HIS PAST MEDICAL HISTORY INCLUDED A RECENT CHEST INFECTION FOR WHICH HE HAD TAKEN A COURSE OF ANTIBIOTICS. HE WAS A SMOKER OF 20 CIGARETTES PER DAY AND DID NOT TAKE ANY REGULAR MEDICATION. ON EXAMINATION HE APPEARED ALERT AND ORIENTATED. THERE APPEARED TO BE GENERALISED REDUCED MUSCLE BULK BUT NO FASCICULATIONS. HIS BLOOD PRESSURE WAS 139/78MMHG, PULSE WAS 67/MIN AND REGULAR AND TEMPERATURE WAS 36.7C. HE HAD MILD BILATERAL PTOSIS HOWEVER OCULAR MOVEMENTS WERE FULL AND THERE WAS NO APPARENT NECK WEAKNESS OR SWALLOWING IMPAIRMENT. ON PERIPHERAL NERVOUS SYSTEM EXAMINATION THE WERE NO OBVIOUS ABNORMALITIES IN THE UPPER LIMB, HOWEVER ON LOWER LIMB EXAMINATION THERE WAS MARKED WEAKNESS OF HIP FLEXION AND EXTENSION, SYMMETRICALLY REDUCED REFLEXES AND NO DEMONSTRABLE SENSORY DISTURBANCES. ON CHEST EXAMINATION HE HAD BILATERAL EXPIRATORY WHEEZE WITH REDUCED AIR ENTRY AND DULL PERCUSSION NOTE IN THE RIGHT LUNG BASE. WHAT IS THE MOST LIKELY DIAGNOSIS?
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A 26-YEAR-OLD FEMALE WHO IS 13 WEEKS PREGNANT IS SEEN IN THE OUTPATIENT CLINIC AND NOTED TO HAVE A SUSTAINED BLOOD PRESSURE OF 170/92 MMHG. SHE HAS NO PAST MEDICAL HISTORY OF NOTE AND HAS OTHERWISE BEEN WELL AND ASYMPTOMATIC. THIS IS HER FIRST PREGNANCY. EXAMINATION IS OTHERWISE GENERALLY NORMAL AND NO ABNORMALITIES ARE NOTED ON FUNDOSCOPY. ULTRASOUND EXAMINATION OF THE KIDNEYS SHOWED BOTH KIDNEYS TO BE OF EQUAL SIZE 9-10 CM. URINALYSIS REVEALS PROTEIN (+) AND BLOOD (+). WHAT IS THE MOST APPROPRIATE ANTI- HYPERTENSIVE THERAPY FOR THIS PATIENT?
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A 29 YEAR-OLD MAN PRESENTED TO HOSPITAL WITH A FOUR WEEK HISTORY OF PROGRESSIVELY WORSENING DYSPNOEA ON EXERTION. HE ALSO COMPLAINED OF A NON-PRODUCTIVE COUGH. OVER THE TWO DAYS PRECEDING ADMISSION THE PATIENT HAD BECOME BREATHLESS AT REST AND WAS STARTED ON ORAL CO-AMOXICLAV BY HIS GENERAL PRACTITIONER. ON EXAMINATION HE WAS FEBRILE 38°C AND LOOKED UNWELL. CANDIDA WAS NOTED
ON THE TONSILAR PILLARS. OXYGEN SATURATION WAS 95% ON ROOM AIR, BUT FELL TO 85% FOLLOWING A BOUT OF COUGHING. NO WHEEZE OR CRACKLES
WERE HEARD IN HIS CHEST. HIS CHEST RADIOGRAPH IS SHOWN. WHAT IS THE MOST LIKELY DIAGNOSIS? (PLEASE SELECT AN OPTION)

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A 47-YEAR-OLD LADY WITH A POSITIVE FAMILY HISTORY OF HYPERTENSION AND PREMATURE CORONARY ARTERY DISEASE IS REFERRED TO THE OUTPATIENT CLINIC FOR ASSESSMENT OF POORLY CONTROLLED HYPERTENSION. HER BLOOD PRESSURE IN CLINIC IS MEASURED AT 200/100 MMHG. AN MRI SCAN OF HER AORTA AND RENAL ARTERIES SHOWS SEVERE ATHEROMATOUS STENOSIS IN BOTH RENAL ARTERIES. WHAT IS BEST WAY OF TREATING HER ELEVATED BLOOD PRESSURE? (PLEASE SELECT AN OPTION)
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A 16-YEAR-OLD BOY WAS ADMITTED TO CASUALTY HAVING SUSTAINED A HEAD INJURY FOLLOWING A COLLISION WITH A PASSING CAR. HE HAD BEEN WALKING AROUND TOWN ALONE DURING THE SCHOOL LUNCH HOUR. A PASSER-BY GAVE A WITNESS ACCOUNT AND SAID THAT HE HAD APPARENTLY STEPPED OUT INTO A BUSY A-ROAD WITHOUT LOOKING. THE WITNESS SAID IT LOOKED AS IF HE DELIBERATELY RAN OUT TO CAUSE THE TRAFFIC TO STOP, AS HE DIDN’T APPEAR STARTLED WHEN THE CAR APPROACHING HIM SWERVED AND HE WAS THROWN OVER THE BONNET. HE SUSTAINED AN OCCIPITAL FRACTURE WITH UNDERLYING HAEMATOMA AND HAD BROKEN BOTH WRISTS. HE HAD NO KNOWN MEDICAL PROBLEMS AND WAS NOT TAKING ANY REGULAR MEDICATION. HE SMOKED 10 CIGARETTES PER DAY AND DRANK 15 UNITS OF ALCOHOL PER WEEK. RECENTLY HE HAD STARTED SMOKING CANNABIS. HE LIVED WITH HIS MOTHER WHO HAD BEEN DIAGNOSED WITH BREAST CARCINOMA SEVERAL MONTHS AGO AND WAS TAKING REGULAR MORPHINE FOR PAIN RELIEF. HE HAD NO CONTACT WITH HIS FATHER AS HE HAD WALKED OUT ON THE FAMILY SEVERAL YEARS AGO. THERE HAD BEEN A CATALOGUE OF AGGRESSIVE EVENTS OVER SEVERAL YEARS AT SCHOOL, WHEREBY HE HAD ASSAULTED A FELLOW PUPIL, AND HAD SET LIGHT TO A RUCKSACK. HE HAD FEW FRIENDS AND APPEARED DETACHED. HIS MOTHER WHOM WAS PRESENT HAD NOT NOTICED ANY CHANGE IN HIS MOOD OR EATING/SLEEPING PATTERN, ALTHOUGH HE WAS RARELY IN THE HOUSE MORE THAN FIVE MINUTES IN THE EVENING. ON EXAMINATION HIS GLASGOW COMA SCALE WAS 13/15 AND HE APPEARED CONFUSED. HE HAD A BOGGY SWELLING OVER THE LEFT OCCIPUT AND SEVERAL CUTS AND BRUISES OVER THE FACE. VITAL SIGNS WERE ALL NORMAL, PUPILS WERE EQUAL AND REACTIVE TO LIGHT AND THERE WERE NO OTHER CRANIAL NERVE ABNORMALITIES. THE PERIPHERAL NERVOUS SYSTEM EXAMINATION WAS ENTIRELY NORMAL AND THERE WAS NO SCARS OR CUTS OVER THE TORSO OR LIMBS. WHAT IS THE LIKELY DIAGNOSIS IN THIS PATIENT? (PLEASE SELECT AN OPTION)
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A 47-YEAR-OLD MAN WITH HIV DISEASE PRESENTS TO HOSPITAL WITH A TONIC-CLONIC SEIZURE. HE HAD INITIALLY PRESENTED SIX MONTHS PREVIOUSLY WITH PNEUMOCYSTIS CARINII PNEUMONIA WITH A CD4 T-LYMPHOCYTE COUNT OF 10 CELLS/MM3 AND HAD SUBSEQUENTLY STARTED ON HIGHLY ACTIVE ANTIRETROVIRAL THERAPY. HIS MOST RECENT CD4 COUNT, TAKEN ONE MONTH PRIOR TO HIS NEW PRESENTATION, WAS 50 CELLS/MM3. ON EXAMINATION HE HAS NO FOCAL WEAKNESS, BUT BOTH PLANTAR RESPONSES ARE EXTENSOR. FUNDOSCOPY IS NORMAL. A CT SCAN OF HIS BRAIN IS SHOWN. WHAT IS THE DIAGNOSIS?

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CASO CLÍNICO SERIADO 1/5

THE PRICE OF BEING A DOCTOR GREG BRATTON, MD I SAW A PATIENT WHILE I WAS MOONLIGHTING THE OTHER NIGHT THAT ACTUALLY MADE ME QUESTION WHETHER OR NOT IT WAS WORTH IT TO BE A DOCTOR. THE PATIENT WAS A 56-YEAR-OLD GENTLEMAN WHO PRESENTED TO THE EMERGENCY ROOM COMPLAINING OF NECK PAIN. WHEN I WENT TO TALK WITH HIM AND LEARN MORE ABOUT HIS COMPLAINT, HE TOLD ME THAT HE HAD A HISTORY OF NECK PAIN AND FELT AS IF IT WAS ABOUT TO START REBOUNDING AGAIN”. HE HAD NO PREVIOUS OR RECENT INJURY TO HIS NECK, NEVER UNDERWENT RADIOGRAPHS, AND HAD NO NEUROLOGICAL SYMPTOMS, BUT SOME PHYSICIAN SOMEWHERE HAD FELT IT WAS APPROPRIATE TO GIVE HIM HYDROCODONE, AND HE HAD BEEN TREATING HIS PAIN EFFECTIVELY” WITH THIS MEDICATION EVER SINCE. HE WAS TAKING NO ANTI-INFLAMATORIES, HAD NEVER SEEN A PHYSICAL THERAPIST, AND HAD TAKEN NO OTHER CONSERVATIVE MEASURES TO MANAGE HIS PAIN. IN FACT, HE HAD NO PRIMARY CARE PHYSICIAN AT ALL. AS WE TALKED, IT BECAME BLATANTLY CLEAR THAT HIS “REBOUNDING PAIN” WAS RUNNING IN DIRECT CORRELATION WITH HIS DWINDLING HYDROCODONE PRESCRIPTION. I READILY ADMIT THAT I BELIEVE WE, AS A WHOLE, UNDER TREAT PAIN (FOR FEAR OF INDUCING POTENTIAL ADDICTION, TOLERANCE, AND SIDE EFFECTS), WICH IS A DISSERVICE TO OUR PATIENTS AND THEIR QUALITY OF LIFE. HOWEVER, AS A SPORTS MEDICINE PHYSICIAN, I SEE MY FAIR SHARE OF CHRONIC MUSCULOSKELETAL PAIN AND, THEREFORE, AM COMFORTABLE WITH MY TREATMENT ALGORITHM AND WITH WHO QUALIFIES FOR NARCOTIC MEDICATIONS THIS GUY DID NOT REQUIRE NARCOTICS. IN FURTHER DISCUSSING HIS CONDITION AND MY MEDICAL OPINION THAT HE NEEDED TO TREAT THE AILMENT RATHER THAN MASKING IT WITH PAIN MEDS, HE BECAME AGITATED (AS YOU COULD IMAGINE) AND DEMANDED HYDROCODONE. “I NEED HYDROCODONE 10/325 AND I NEED A QUANTITY OF 30”, HE EMPHATICALLY STATED. “IT IS THE ONLY THING THAT WORKS”. AT THIS POINT MY PATIENCE WAS WEARING THIN. NOT ONLY WAS THIS PATIENT MISUSING THE MEDICAL SYSTEM BY ARRIVING AT AN EMERGENCY DEPARTMENT FOR WHAT APPEARED TO BE A MEDICATION REFILL, HE WAS NOW ATTEMPTING TO BULLY ME INTO PRESCRIBING HIM MEDICATION I DID NOT FEEL WAS MEDICALLY NECESSARY. TO MAKE A LONG STORY SHORT, I TOLD THE PATIENT THAT THIS WAS NOT A NEGOTIATION AND THAT I WAS GOING TO TREAT HIM NO DIFFERENTLY THAN I TREAT ANY OF MY OTHER PATIENTS. I STAYED TRUE TO MY CLINICAL CRITERIA FOR PRESCRIBING NARCOTICS, AND HE LEFT WITH A SCRIPT FOR MOBIC. I WAS LATER INFORMED BY MY NURSE THAT, AS HE WAS LEAVING, HE TURNED TO HER AND ASKED, “WHAT NIGHT DOES THAT DOCTOR NOT WORK?” AS IF HE WAS PLOTTING HIS NEXT ATTACK. I WENT BACK TO MY DESK, IRRITATED, AND REFLECTED ABOUT HOW I SPENT 4 YEARS OF MEDICAL SCHOOL, INCURRED A LARGE AMOUNT OF DEBT, TRUDGED THROUGH RESIDENCY, SACRIFICED FAMILY TIME TO EXTEND MY TRAINING THROUGH MOONLIGHTING, PAID BIG BUCKS TO TAKE A BOARD EXAM – NOT TO MENTION THE COST OF LICENSING, DEA, AND DPS NUMBERS- AND HOW IT WAS ALL JUST LOST ON THIS PATIENT BECAUSE I WAS EXPECTED TO DO WHAT HE WANTED. AND TO BE QUITE HONEST, IT PISSED ME OFF. THERE ARE PEOPLE IN OUR COMMUNITIES THAT HAVE CAPITALIZED ON PHYSICIANS FEARS OF LITIGATION AND WILLINGNESS TO PRACTICE DEFENSIVE MEDICINE TO GET WHAT THEY WANT. THEY FEEL ENTITLED WHEN THEY ARE SEEN BY A DOCTOR. THEY “KNOW” WHAT IS MEDICALLY BEST. THEY AREN’T COMING TO THEIR APPOINTMENTS TO GET EVALUATED AND TREATED, BUT RATHER, THEY ARE USING THE DOCTORS AS SUPPLIERS. THEY ARE SUCCESSFUL BECAUSE THEY INSTILL A SENSE OF “IF YOU DON’T DO WHAT I WANT, I WILL REPORT YOU FOR FAILURE TO TREAT MY PAIN ADEQUATELY”. AND IF THIS IS HOW PRACTICING MEDICINE IS GOING TO EVOLVE (INSERT POLITICAL COMMENTARY HERE), THEN IS IT STILL WORTH IT TO BE A DOCTOR??. I HAD THIS QUESTION ANSWERED FOR ME ON EASTER SUNDAY. I WAS ENJOYING A NICE EASTER SERVICE WITH FAMILY. I HAD JUST RETURNED TO MY PEW AFTER COMMUNION WHEN FROM THE BACK OF THE SANCTUARY, A HYSTERICAL MOTHER CALLED OUT, “IS THERE A DOCTOR IN THE HOUSE!??” A SILENCE FELL OVER THE CONGREGATION AND EVERY STOOD FROZEN IN THEIR PLACE – EXCEPT FOR ME. I AROSE FROM MY PEW AND MADE MY WAY TO THE MOTHER. AS I APPROACHED THE WOMAN, I FOUND HER 14-YEAR-OLD DAUGHTER LYING HORIZONTAL ON THE WOODEN PEW, PALE AND DIAPHORETIC WITH A CONFUSED AND SCARED LOOK ON HER FACE. SHE HAD PASSED OUT AND WAS JUST AWAKENING WHEN ARRIVED. WITH THE HELP OF SOME HAD PASSED OUT AND WAS JUST AWAKENING WHEN I ARRIVED. WITH THE HELP OF SOME OTHER PROVIDERS, WE TENDED TO THE YOUNG GIRL, COMFORTED THE MOM, AND HANDLED THE SITUATION APPROPRIATELY. THANKFULLY, THE MOTHERS CALL FOR HELP WAS FOR SOMETHING MINOR, BUT, TO ME, IT WAS A MAJOR BOOST TO MY FAILING SENSE OF PURPOSE. TO HAVE MY “NAME” CALLED IN A MOMENT OF PERSONAL DESPAIR AND TO REALIZE THAT, IN A GATHERING OF 300 OR MORE PEOPLE, I WAS THE ONLY PHYSICIAN, MADE ME FEEL AS IF BEING A PHYSICIAN STILL WAS SOMETHING SPECIAL.

SO, IS IT WORTH IT? YES, IT’S PRICELESS

WHAT DID CAUSE THE DOCTOR FELT IT WAS WORTH TO BE A DOCTOR?.
SELECCIONE UNA:

CASO CLÍNICO SERIADO 2/5

THE PRICE OF BEING A DOCTOR GREG BRATTON, MD I SAW A PATIENT WHILE I WAS MOONLIGHTING THE OTHER NIGHT THAT ACTUALLY MADE ME QUESTION WHETHER OR NOT IT WAS WORTH IT TO BE A DOCTOR. THE PATIENT WAS A 56-YEAR-OLD GENTLEMAN WHO PRESENTED TO THE EMERGENCY ROOM COMPLAINING OF NECK PAIN. WHEN I WENT TO TALK WITH HIM AND LEARN MORE ABOUT HIS COMPLAINT, HE TOLD ME THAT HE HAD A HISTORY OF NECK PAIN AND FELT AS IF IT WAS ABOUT TO START REBOUNDING AGAIN”. HE HAD NO PREVIOUS OR RECENT INJURY TO HIS NECK, NEVER UNDERWENT RADIOGRAPHS, AND HAD NO NEUROLOGICAL SYMPTOMS, BUT SOME PHYSICIAN SOMEWHERE HAD FELT IT WAS APPROPRIATE TO GIVE HIM HYDROCODONE, AND HE HAD BEEN TREATING HIS PAIN EFFECTIVELY” WITH THIS MEDICATION EVER SINCE. HE WAS TAKING NO ANTI-INFLAMATORIES, HAD NEVER SEEN A PHYSICAL THERAPIST, AND HAD TAKEN NO OTHER CONSERVATIVE MEASURES TO MANAGE HIS PAIN. IN FACT, HE HAD NO PRIMARY CARE PHYSICIAN AT ALL. AS WE TALKED, IT BECAME BLATANTLY CLEAR THAT HIS “REBOUNDING PAIN” WAS RUNNING IN DIRECT CORRELATION WITH HIS DWINDLING HYDROCODONE PRESCRIPTION. I READILY ADMIT THAT I BELIEVE WE, AS A WHOLE, UNDER TREAT PAIN (FOR FEAR OF INDUCING POTENTIAL ADDICTION, TOLERANCE, AND SIDE EFFECTS), WICH IS A DISSERVICE TO OUR PATIENTS AND THEIR QUALITY OF LIFE. HOWEVER, AS A SPORTS MEDICINE PHYSICIAN, I SEE MY FAIR SHARE OF CHRONIC MUSCULOSKELETAL PAIN AND, THEREFORE, AM COMFORTABLE WITH MY TREATMENT ALGORITHM AND WITH WHO QUALIFIES FOR NARCOTIC MEDICATIONS THIS GUY DID NOT REQUIRE NARCOTICS. IN FURTHER DISCUSSING HIS CONDITION AND MY MEDICAL OPINION THAT HE NEEDED TO TREAT THE AILMENT RATHER THAN MASKING IT WITH PAIN MEDS, HE BECAME AGITATED (AS YOU COULD IMAGINE) AND DEMANDED HYDROCODONE. “I NEED HYDROCODONE 10/325 AND I NEED A QUANTITY OF 30”, HE EMPHATICALLY STATED. “IT IS THE ONLY THING THAT WORKS”. AT THIS POINT MY PATIENCE WAS WEARING THIN. NOT ONLY WAS THIS PATIENT MISUSING THE MEDICAL SYSTEM BY ARRIVING AT AN EMERGENCY DEPARTMENT FOR WHAT APPEARED TO BE A MEDICATION REFILL, HE WAS NOW ATTEMPTING TO BULLY ME INTO PRESCRIBING HIM MEDICATION I DID NOT FEEL WAS MEDICALLY NECESSARY. TO MAKE A LONG STORY SHORT, I TOLD THE PATIENT THAT THIS WAS NOT A NEGOTIATION AND THAT I WAS GOING TO TREAT HIM NO DIFFERENTLY THAN I TREAT ANY OF MY OTHER PATIENTS. I STAYED TRUE TO MY CLINICAL CRITERIA FOR PRESCRIBING NARCOTICS, AND HE LEFT WITH A SCRIPT FOR MOBIC. I WAS LATER INFORMED BY MY NURSE THAT, AS HE WAS LEAVING, HE TURNED TO HER AND ASKED, “WHAT NIGHT DOES THAT DOCTOR NOT WORK?” AS IF HE WAS PLOTTING HIS NEXT ATTACK. I WENT BACK TO MY DESK, IRRITATED, AND REFLECTED ABOUT HOW I SPENT 4 YEARS OF MEDICAL SCHOOL, INCURRED A LARGE AMOUNT OF DEBT, TRUDGED THROUGH RESIDENCY, SACRIFICED FAMILY TIME TO EXTEND MY TRAINING THROUGH MOONLIGHTING, PAID BIG BUCKS TO TAKE A BOARD EXAM – NOT TO MENTION THE COST OF LICENSING, DEA, AND DPS NUMBERS- AND HOW IT WAS ALL JUST LOST ON THIS PATIENT BECAUSE I WAS EXPECTED TO DO WHAT HE WANTED. AND TO BE QUITE HONEST, IT PISSED ME OFF. THERE ARE PEOPLE IN OUR COMMUNITIES THAT HAVE CAPITALIZED ON PHYSICIANS FEARS OF LITIGATION AND WILLINGNESS TO PRACTICE DEFENSIVE MEDICINE TO GET WHAT THEY WANT. THEY FEEL ENTITLED WHEN THEY ARE SEEN BY A DOCTOR. THEY “KNOW” WHAT IS MEDICALLY BEST. THEY AREN’T COMING TO THEIR APPOINTMENTS TO GET EVALUATED AND TREATED, BUT RATHER, THEY ARE USING THE DOCTORS AS SUPPLIERS. THEY ARE SUCCESSFUL BECAUSE THEY INSTILL A SENSE OF “IF YOU DON’T DO WHAT I WANT, I WILL REPORT YOU FOR FAILURE TO TREAT MY PAIN ADEQUATELY”. AND IF THIS IS HOW PRACTICING MEDICINE IS GOING TO EVOLVE (INSERT POLITICAL COMMENTARY HERE), THEN IS IT STILL WORTH IT TO BE A DOCTOR??. I HAD THIS QUESTION ANSWERED FOR ME ON EASTER SUNDAY. I WAS ENJOYING A NICE EASTER SERVICE WITH FAMILY. I HAD JUST RETURNED TO MY PEW AFTER COMMUNION WHEN FROM THE BACK OF THE SANCTUARY, A HYSTERICAL MOTHER CALLED OUT, “IS THERE A DOCTOR IN THE HOUSE!??” A SILENCE FELL OVER THE CONGREGATION AND EVERY STOOD FROZEN IN THEIR PLACE – EXCEPT FOR ME. I AROSE FROM MY PEW AND MADE MY WAY TO THE MOTHER. AS I APPROACHED THE WOMAN, I FOUND HER 14-YEAR-OLD DAUGHTER LYING HORIZONTAL ON THE WOODEN PEW, PALE AND DIAPHORETIC WITH A CONFUSED AND SCARED LOOK ON HER FACE. SHE HAD PASSED OUT AND WAS JUST AWAKENING WHEN ARRIVED. WITH THE HELP OF SOME HAD PASSED OUT AND WAS JUST AWAKENING WHEN I ARRIVED. WITH THE HELP OF SOME OTHER PROVIDERS, WE TENDED TO THE YOUNG GIRL, COMFORTED THE MOM, AND HANDLED THE SITUATION APPROPRIATELY. THANKFULLY, THE MOTHERS CALL FOR HELP WAS FOR SOMETHING MINOR, BUT, TO ME, IT WAS A MAJOR BOOST TO MY FAILING SENSE OF PURPOSE. TO HAVE MY “NAME” CALLED IN A MOMENT OF PERSONAL DESPAIR AND TO REALIZE THAT, IN A GATHERING OF 300 OR MORE PEOPLE, I WAS THE ONLY PHYSICIAN, MADE ME FEEL AS IF BEING A PHYSICIAN STILL WAS SOMETHING SPECIAL.

SO, IS IT WORTH IT? YES, IT’S PRICELESS

WHICH WAS THE INITIAL DISAGREEMENT WITH THE PATIENT WHO HAD NECK PAIN?
SELECCIONE UNA:

CASO CLÍNICO SERIADO 3/5

THE PRICE OF BEING A DOCTOR GREG BRATTON, MD I SAW A PATIENT WHILE I WAS MOONLIGHTING THE OTHER NIGHT THAT ACTUALLY MADE ME QUESTION WHETHER OR NOT IT WAS WORTH IT TO BE A DOCTOR. THE PATIENT WAS A 56-YEAR-OLD GENTLEMAN WHO PRESENTED TO THE EMERGENCY ROOM COMPLAINING OF NECK PAIN. WHEN I WENT TO TALK WITH HIM AND LEARN MORE ABOUT HIS COMPLAINT, HE TOLD ME THAT HE HAD A HISTORY OF NECK PAIN AND FELT AS IF IT WAS ABOUT TO START REBOUNDING AGAIN”. HE HAD NO PREVIOUS OR RECENT INJURY TO HIS NECK, NEVER UNDERWENT RADIOGRAPHS, AND HAD NO NEUROLOGICAL SYMPTOMS, BUT SOME PHYSICIAN SOMEWHERE HAD FELT IT WAS APPROPRIATE TO GIVE HIM HYDROCODONE, AND HE HAD BEEN TREATING HIS PAIN EFFECTIVELY” WITH THIS MEDICATION EVER SINCE. HE WAS TAKING NO ANTI-INFLAMATORIES, HAD NEVER SEEN A PHYSICAL THERAPIST, AND HAD TAKEN NO OTHER CONSERVATIVE MEASURES TO MANAGE HIS PAIN. IN FACT, HE HAD NO PRIMARY CARE PHYSICIAN AT ALL. AS WE TALKED, IT BECAME BLATANTLY CLEAR THAT HIS “REBOUNDING PAIN” WAS RUNNING IN DIRECT CORRELATION WITH HIS DWINDLING HYDROCODONE PRESCRIPTION. I READILY ADMIT THAT I BELIEVE WE, AS A WHOLE, UNDER TREAT PAIN (FOR FEAR OF INDUCING POTENTIAL ADDICTION, TOLERANCE, AND SIDE EFFECTS), WICH IS A DISSERVICE TO OUR PATIENTS AND THEIR QUALITY OF LIFE. HOWEVER, AS A SPORTS MEDICINE PHYSICIAN, I SEE MY FAIR SHARE OF CHRONIC MUSCULOSKELETAL PAIN AND, THEREFORE, AM COMFORTABLE WITH MY TREATMENT ALGORITHM AND WITH WHO QUALIFIES FOR NARCOTIC MEDICATIONS THIS GUY DID NOT REQUIRE NARCOTICS. IN FURTHER DISCUSSING HIS CONDITION AND MY MEDICAL OPINION THAT HE NEEDED TO TREAT THE AILMENT RATHER THAN MASKING IT WITH PAIN MEDS, HE BECAME AGITATED (AS YOU COULD IMAGINE) AND DEMANDED HYDROCODONE. “I NEED HYDROCODONE 10/325 AND I NEED A QUANTITY OF 30”, HE EMPHATICALLY STATED. “IT IS THE ONLY THING THAT WORKS”. AT THIS POINT MY PATIENCE WAS WEARING THIN. NOT ONLY WAS THIS PATIENT MISUSING THE MEDICAL SYSTEM BY ARRIVING AT AN EMERGENCY DEPARTMENT FOR WHAT APPEARED TO BE A MEDICATION REFILL, HE WAS NOW ATTEMPTING TO BULLY ME INTO PRESCRIBING HIM MEDICATION I DID NOT FEEL WAS MEDICALLY NECESSARY. TO MAKE A LONG STORY SHORT, I TOLD THE PATIENT THAT THIS WAS NOT A NEGOTIATION AND THAT I WAS GOING TO TREAT HIM NO DIFFERENTLY THAN I TREAT ANY OF MY OTHER PATIENTS. I STAYED TRUE TO MY CLINICAL CRITERIA FOR PRESCRIBING NARCOTICS, AND HE LEFT WITH A SCRIPT FOR MOBIC. I WAS LATER INFORMED BY MY NURSE THAT, AS HE WAS LEAVING, HE TURNED TO HER AND ASKED, “WHAT NIGHT DOES THAT DOCTOR NOT WORK?” AS IF HE WAS PLOTTING HIS NEXT ATTACK. I WENT BACK TO MY DESK, IRRITATED, AND REFLECTED ABOUT HOW I SPENT 4 YEARS OF MEDICAL SCHOOL, INCURRED A LARGE AMOUNT OF DEBT, TRUDGED THROUGH RESIDENCY, SACRIFICED FAMILY TIME TO EXTEND MY TRAINING THROUGH MOONLIGHTING, PAID BIG BUCKS TO TAKE A BOARD EXAM – NOT TO MENTION THE COST OF LICENSING, DEA, AND DPS NUMBERS- AND HOW IT WAS ALL JUST LOST ON THIS PATIENT BECAUSE I WAS EXPECTED TO DO WHAT HE WANTED. AND TO BE QUITE HONEST, IT PISSED ME OFF. THERE ARE PEOPLE IN OUR COMMUNITIES THAT HAVE CAPITALIZED ON PHYSICIANS FEARS OF LITIGATION AND WILLINGNESS TO PRACTICE DEFENSIVE MEDICINE TO GET WHAT THEY WANT. THEY FEEL ENTITLED WHEN THEY ARE SEEN BY A DOCTOR. THEY “KNOW” WHAT IS MEDICALLY BEST. THEY AREN’T COMING TO THEIR APPOINTMENTS TO GET EVALUATED AND TREATED, BUT RATHER, THEY ARE USING THE DOCTORS AS SUPPLIERS. THEY ARE SUCCESSFUL BECAUSE THEY INSTILL A SENSE OF “IF YOU DON’T DO WHAT I WANT, I WILL REPORT YOU FOR FAILURE TO TREAT MY PAIN ADEQUATELY”. AND IF THIS IS HOW PRACTICING MEDICINE IS GOING TO EVOLVE (INSERT POLITICAL COMMENTARY HERE), THEN IS IT STILL WORTH IT TO BE A DOCTOR??. I HAD THIS QUESTION ANSWERED FOR ME ON EASTER SUNDAY. I WAS ENJOYING A NICE EASTER SERVICE WITH FAMILY. I HAD JUST RETURNED TO MY PEW AFTER COMMUNION WHEN FROM THE BACK OF THE SANCTUARY, A HYSTERICAL MOTHER CALLED OUT, “IS THERE A DOCTOR IN THE HOUSE!??” A SILENCE FELL OVER THE CONGREGATION AND EVERY STOOD FROZEN IN THEIR PLACE – EXCEPT FOR ME. I AROSE FROM MY PEW AND MADE MY WAY TO THE MOTHER. AS I APPROACHED THE WOMAN, I FOUND HER 14-YEAR-OLD DAUGHTER LYING HORIZONTAL ON THE WOODEN PEW, PALE AND DIAPHORETIC WITH A CONFUSED AND SCARED LOOK ON HER FACE. SHE HAD PASSED OUT AND WAS JUST AWAKENING WHEN ARRIVED. WITH THE HELP OF SOME HAD PASSED OUT AND WAS JUST AWAKENING WHEN I ARRIVED. WITH THE HELP OF SOME OTHER PROVIDERS, WE TENDED TO THE YOUNG GIRL, COMFORTED THE MOM, AND HANDLED THE SITUATION APPROPRIATELY. THANKFULLY, THE MOTHERS CALL FOR HELP WAS FOR SOMETHING MINOR, BUT, TO ME, IT WAS A MAJOR BOOST TO MY FAILING SENSE OF PURPOSE. TO HAVE MY “NAME” CALLED IN A MOMENT OF PERSONAL DESPAIR AND TO REALIZE THAT, IN A GATHERING OF 300 OR MORE PEOPLE, I WAS THE ONLY PHYSICIAN, MADE ME FEEL AS IF BEING A PHYSICIAN STILL WAS SOMETHING SPECIAL.

SO, IS IT WORTH IT? YES, IT’S PRICELESS

WHAT IS THE REASON WHY MANY DOCTORS GIVE IN TO THE DEMANDS OF THEIR PATIENTS?
SELECCIONE UNA:

CASO CLÍNICO SERIADO 4/5

THE PRICE OF BEING A DOCTOR GREG BRATTON, MD I SAW A PATIENT WHILE I WAS MOONLIGHTING THE OTHER NIGHT THAT ACTUALLY MADE ME QUESTION WHETHER OR NOT IT WAS WORTH IT TO BE A DOCTOR. THE PATIENT WAS A 56-YEAR-OLD GENTLEMAN WHO PRESENTED TO THE EMERGENCY ROOM COMPLAINING OF NECK PAIN. WHEN I WENT TO TALK WITH HIM AND LEARN MORE ABOUT HIS COMPLAINT, HE TOLD ME THAT HE HAD A HISTORY OF NECK PAIN AND FELT AS IF IT WAS ABOUT TO START REBOUNDING AGAIN”. HE HAD NO PREVIOUS OR RECENT INJURY TO HIS NECK, NEVER UNDERWENT RADIOGRAPHS, AND HAD NO NEUROLOGICAL SYMPTOMS, BUT SOME PHYSICIAN SOMEWHERE HAD FELT IT WAS APPROPRIATE TO GIVE HIM HYDROCODONE, AND HE HAD BEEN TREATING HIS PAIN EFFECTIVELY” WITH THIS MEDICATION EVER SINCE. HE WAS TAKING NO ANTI-INFLAMATORIES, HAD NEVER SEEN A PHYSICAL THERAPIST, AND HAD TAKEN NO OTHER CONSERVATIVE MEASURES TO MANAGE HIS PAIN. IN FACT, HE HAD NO PRIMARY CARE PHYSICIAN AT ALL. AS WE TALKED, IT BECAME BLATANTLY CLEAR THAT HIS “REBOUNDING PAIN” WAS RUNNING IN DIRECT CORRELATION WITH HIS DWINDLING HYDROCODONE PRESCRIPTION. I READILY ADMIT THAT I BELIEVE WE, AS A WHOLE, UNDER TREAT PAIN (FOR FEAR OF INDUCING POTENTIAL ADDICTION, TOLERANCE, AND SIDE EFFECTS), WICH IS A DISSERVICE TO OUR PATIENTS AND THEIR QUALITY OF LIFE. HOWEVER, AS A SPORTS MEDICINE PHYSICIAN, I SEE MY FAIR SHARE OF CHRONIC MUSCULOSKELETAL PAIN AND, THEREFORE, AM COMFORTABLE WITH MY TREATMENT ALGORITHM AND WITH WHO QUALIFIES FOR NARCOTIC MEDICATIONS THIS GUY DID NOT REQUIRE NARCOTICS. IN FURTHER DISCUSSING HIS CONDITION AND MY MEDICAL OPINION THAT HE NEEDED TO TREAT THE AILMENT RATHER THAN MASKING IT WITH PAIN MEDS, HE BECAME AGITATED (AS YOU COULD IMAGINE) AND DEMANDED HYDROCODONE. “I NEED HYDROCODONE 10/325 AND I NEED A QUANTITY OF 30”, HE EMPHATICALLY STATED. “IT IS THE ONLY THING THAT WORKS”. AT THIS POINT MY PATIENCE WAS WEARING THIN. NOT ONLY WAS THIS PATIENT MISUSING THE MEDICAL SYSTEM BY ARRIVING AT AN EMERGENCY DEPARTMENT FOR WHAT APPEARED TO BE A MEDICATION REFILL, HE WAS NOW ATTEMPTING TO BULLY ME INTO PRESCRIBING HIM MEDICATION I DID NOT FEEL WAS MEDICALLY NECESSARY. TO MAKE A LONG STORY SHORT, I TOLD THE PATIENT THAT THIS WAS NOT A NEGOTIATION AND THAT I WAS GOING TO TREAT HIM NO DIFFERENTLY THAN I TREAT ANY OF MY OTHER PATIENTS. I STAYED TRUE TO MY CLINICAL CRITERIA FOR PRESCRIBING NARCOTICS, AND HE LEFT WITH A SCRIPT FOR MOBIC. I WAS LATER INFORMED BY MY NURSE THAT, AS HE WAS LEAVING, HE TURNED TO HER AND ASKED, “WHAT NIGHT DOES THAT DOCTOR NOT WORK?” AS IF HE WAS PLOTTING HIS NEXT ATTACK. I WENT BACK TO MY DESK, IRRITATED, AND REFLECTED ABOUT HOW I SPENT 4 YEARS OF MEDICAL SCHOOL, INCURRED A LARGE AMOUNT OF DEBT, TRUDGED THROUGH RESIDENCY, SACRIFICED FAMILY TIME TO EXTEND MY TRAINING THROUGH MOONLIGHTING, PAID BIG BUCKS TO TAKE A BOARD EXAM – NOT TO MENTION THE COST OF LICENSING, DEA, AND DPS NUMBERS- AND HOW IT WAS ALL JUST LOST ON THIS PATIENT BECAUSE I WAS EXPECTED TO DO WHAT HE WANTED. AND TO BE QUITE HONEST, IT PISSED ME OFF. THERE ARE PEOPLE IN OUR COMMUNITIES THAT HAVE CAPITALIZED ON PHYSICIANS FEARS OF LITIGATION AND WILLINGNESS TO PRACTICE DEFENSIVE MEDICINE TO GET WHAT THEY WANT. THEY FEEL ENTITLED WHEN THEY ARE SEEN BY A DOCTOR. THEY “KNOW” WHAT IS MEDICALLY BEST. THEY AREN’T COMING TO THEIR APPOINTMENTS TO GET EVALUATED AND TREATED, BUT RATHER, THEY ARE USING THE DOCTORS AS SUPPLIERS. THEY ARE SUCCESSFUL BECAUSE THEY INSTILL A SENSE OF “IF YOU DON’T DO WHAT I WANT, I WILL REPORT YOU FOR FAILURE TO TREAT MY PAIN ADEQUATELY”. AND IF THIS IS HOW PRACTICING MEDICINE IS GOING TO EVOLVE (INSERT POLITICAL COMMENTARY HERE), THEN IS IT STILL WORTH IT TO BE A DOCTOR??. I HAD THIS QUESTION ANSWERED FOR ME ON EASTER SUNDAY. I WAS ENJOYING A NICE EASTER SERVICE WITH FAMILY. I HAD JUST RETURNED TO MY PEW AFTER COMMUNION WHEN FROM THE BACK OF THE SANCTUARY, A HYSTERICAL MOTHER CALLED OUT, “IS THERE A DOCTOR IN THE HOUSE!??” A SILENCE FELL OVER THE CONGREGATION AND EVERY STOOD FROZEN IN THEIR PLACE – EXCEPT FOR ME. I AROSE FROM MY PEW AND MADE MY WAY TO THE MOTHER. AS I APPROACHED THE WOMAN, I FOUND HER 14-YEAR-OLD DAUGHTER LYING HORIZONTAL ON THE WOODEN PEW, PALE AND DIAPHORETIC WITH A CONFUSED AND SCARED LOOK ON HER FACE. SHE HAD PASSED OUT AND WAS JUST AWAKENING WHEN ARRIVED. WITH THE HELP OF SOME HAD PASSED OUT AND WAS JUST AWAKENING WHEN I ARRIVED. WITH THE HELP OF SOME OTHER PROVIDERS, WE TENDED TO THE YOUNG GIRL, COMFORTED THE MOM, AND HANDLED THE SITUATION APPROPRIATELY. THANKFULLY, THE MOTHERS CALL FOR HELP WAS FOR SOMETHING MINOR, BUT, TO ME, IT WAS A MAJOR BOOST TO MY FAILING SENSE OF PURPOSE. TO HAVE MY “NAME” CALLED IN A MOMENT OF PERSONAL DESPAIR AND TO REALIZE THAT, IN A GATHERING OF 300 OR MORE PEOPLE, I WAS THE ONLY PHYSICIAN, MADE ME FEEL AS IF BEING A PHYSICIAN STILL WAS SOMETHING SPECIAL.

SO, IS IT WORTH IT? YES, IT’S PRICELESS

YOU CONSIDER THAT THE CONDUCT WAS APPROPRIATE
SELECCIONE UNA:

CASO CLÍNICO SERIADO 5/5

THE PRICE OF BEING A DOCTOR GREG BRATTON, MD I SAW A PATIENT WHILE I WAS MOONLIGHTING THE OTHER NIGHT THAT ACTUALLY MADE ME QUESTION WHETHER OR NOT IT WAS WORTH IT TO BE A DOCTOR. THE PATIENT WAS A 56-YEAR-OLD GENTLEMAN WHO PRESENTED TO THE EMERGENCY ROOM COMPLAINING OF NECK PAIN. WHEN I WENT TO TALK WITH HIM AND LEARN MORE ABOUT HIS COMPLAINT, HE TOLD ME THAT HE HAD A HISTORY OF NECK PAIN AND FELT AS IF IT WAS ABOUT TO START REBOUNDING AGAIN”. HE HAD NO PREVIOUS OR RECENT INJURY TO HIS NECK, NEVER UNDERWENT RADIOGRAPHS, AND HAD NO NEUROLOGICAL SYMPTOMS, BUT SOME PHYSICIAN SOMEWHERE HAD FELT IT WAS APPROPRIATE TO GIVE HIM HYDROCODONE, AND HE HAD BEEN TREATING HIS PAIN EFFECTIVELY” WITH THIS MEDICATION EVER SINCE. HE WAS TAKING NO ANTI-INFLAMATORIES, HAD NEVER SEEN A PHYSICAL THERAPIST, AND HAD TAKEN NO OTHER CONSERVATIVE MEASURES TO MANAGE HIS PAIN. IN FACT, HE HAD NO PRIMARY CARE PHYSICIAN AT ALL. AS WE TALKED, IT BECAME BLATANTLY CLEAR THAT HIS “REBOUNDING PAIN” WAS RUNNING IN DIRECT CORRELATION WITH HIS DWINDLING HYDROCODONE PRESCRIPTION. I READILY ADMIT THAT I BELIEVE WE, AS A WHOLE, UNDER TREAT PAIN (FOR FEAR OF INDUCING POTENTIAL ADDICTION, TOLERANCE, AND SIDE EFFECTS), WICH IS A DISSERVICE TO OUR PATIENTS AND THEIR QUALITY OF LIFE. HOWEVER, AS A SPORTS MEDICINE PHYSICIAN, I SEE MY FAIR SHARE OF CHRONIC MUSCULOSKELETAL PAIN AND, THEREFORE, AM COMFORTABLE WITH MY TREATMENT ALGORITHM AND WITH WHO QUALIFIES FOR NARCOTIC MEDICATIONS THIS GUY DID NOT REQUIRE NARCOTICS. IN FURTHER DISCUSSING HIS CONDITION AND MY MEDICAL OPINION THAT HE NEEDED TO TREAT THE AILMENT RATHER THAN MASKING IT WITH PAIN MEDS, HE BECAME AGITATED (AS YOU COULD IMAGINE) AND DEMANDED HYDROCODONE. “I NEED HYDROCODONE 10/325 AND I NEED A QUANTITY OF 30”, HE EMPHATICALLY STATED. “IT IS THE ONLY THING THAT WORKS”. AT THIS POINT MY PATIENCE WAS WEARING THIN. NOT ONLY WAS THIS PATIENT MISUSING THE MEDICAL SYSTEM BY ARRIVING AT AN EMERGENCY DEPARTMENT FOR WHAT APPEARED TO BE A MEDICATION REFILL, HE WAS NOW ATTEMPTING TO BULLY ME INTO PRESCRIBING HIM MEDICATION I DID NOT FEEL WAS MEDICALLY NECESSARY. TO MAKE A LONG STORY SHORT, I TOLD THE PATIENT THAT THIS WAS NOT A NEGOTIATION AND THAT I WAS GOING TO TREAT HIM NO DIFFERENTLY THAN I TREAT ANY OF MY OTHER PATIENTS. I STAYED TRUE TO MY CLINICAL CRITERIA FOR PRESCRIBING NARCOTICS, AND HE LEFT WITH A SCRIPT FOR MOBIC. I WAS LATER INFORMED BY MY NURSE THAT, AS HE WAS LEAVING, HE TURNED TO HER AND ASKED, “WHAT NIGHT DOES THAT DOCTOR NOT WORK?” AS IF HE WAS PLOTTING HIS NEXT ATTACK. I WENT BACK TO MY DESK, IRRITATED, AND REFLECTED ABOUT HOW I SPENT 4 YEARS OF MEDICAL SCHOOL, INCURRED A LARGE AMOUNT OF DEBT, TRUDGED THROUGH RESIDENCY, SACRIFICED FAMILY TIME TO EXTEND MY TRAINING THROUGH MOONLIGHTING, PAID BIG BUCKS TO TAKE A BOARD EXAM – NOT TO MENTION THE COST OF LICENSING, DEA, AND DPS NUMBERS- AND HOW IT WAS ALL JUST LOST ON THIS PATIENT BECAUSE I WAS EXPECTED TO DO WHAT HE WANTED. AND TO BE QUITE HONEST, IT PISSED ME OFF. THERE ARE PEOPLE IN OUR COMMUNITIES THAT HAVE CAPITALIZED ON PHYSICIANS FEARS OF LITIGATION AND WILLINGNESS TO PRACTICE DEFENSIVE MEDICINE TO GET WHAT THEY WANT. THEY FEEL ENTITLED WHEN THEY ARE SEEN BY A DOCTOR. THEY “KNOW” WHAT IS MEDICALLY BEST. THEY AREN’T COMING TO THEIR APPOINTMENTS TO GET EVALUATED AND TREATED, BUT RATHER, THEY ARE USING THE DOCTORS AS SUPPLIERS. THEY ARE SUCCESSFUL BECAUSE THEY INSTILL A SENSE OF “IF YOU DON’T DO WHAT I WANT, I WILL REPORT YOU FOR FAILURE TO TREAT MY PAIN ADEQUATELY”. AND IF THIS IS HOW PRACTICING MEDICINE IS GOING TO EVOLVE (INSERT POLITICAL COMMENTARY HERE), THEN IS IT STILL WORTH IT TO BE A DOCTOR??. I HAD THIS QUESTION ANSWERED FOR ME ON EASTER SUNDAY. I WAS ENJOYING A NICE EASTER SERVICE WITH FAMILY. I HAD JUST RETURNED TO MY PEW AFTER COMMUNION WHEN FROM THE BACK OF THE SANCTUARY, A HYSTERICAL MOTHER CALLED OUT, “IS THERE A DOCTOR IN THE HOUSE!??” A SILENCE FELL OVER THE CONGREGATION AND EVERY STOOD FROZEN IN THEIR PLACE – EXCEPT FOR ME. I AROSE FROM MY PEW AND MADE MY WAY TO THE MOTHER. AS I APPROACHED THE WOMAN, I FOUND HER 14-YEAR-OLD DAUGHTER LYING HORIZONTAL ON THE WOODEN PEW, PALE AND DIAPHORETIC WITH A CONFUSED AND SCARED LOOK ON HER FACE. SHE HAD PASSED OUT AND WAS JUST AWAKENING WHEN ARRIVED. WITH THE HELP OF SOME HAD PASSED OUT AND WAS JUST AWAKENING WHEN I ARRIVED. WITH THE HELP OF SOME OTHER PROVIDERS, WE TENDED TO THE YOUNG GIRL, COMFORTED THE MOM, AND HANDLED THE SITUATION APPROPRIATELY. THANKFULLY, THE MOTHERS CALL FOR HELP WAS FOR SOMETHING MINOR, BUT, TO ME, IT WAS A MAJOR BOOST TO MY FAILING SENSE OF PURPOSE. TO HAVE MY “NAME” CALLED IN A MOMENT OF PERSONAL DESPAIR AND TO REALIZE THAT, IN A GATHERING OF 300 OR MORE PEOPLE, I WAS THE ONLY PHYSICIAN, MADE ME FEEL AS IF BEING A PHYSICIAN STILL WAS SOMETHING SPECIAL.

SO, IS IT WORTH IT? YES, IT’S PRICELESS

IN SOME COMMUNITIES, PHYSICIANS ARE BEING USED AS:
SELECCIONE UNA:

CASO CLÍNICO SERIADO 2/5

CAROTID-WALL INTIMA-MEDIA THICKNESS AND CARDIOVASCULAR EVENTS

JOSEPH F. POLAK, N ENGL J MED 2011; 365:213-221 JULY 21, 2011

BACKGROUND. INTIMA-MEDIA THICKNESS OF THE WALLS OF THE COMMON CAROTID ARTERY AND INTERNAL CAROTID ARTERY MAY ADD TO THE FRAMINGHAM RISK SCORE FOR PREDICTING CARDIOVASCULAR EVENTS.

METHODS. WE MEASURED THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY AND THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNA CAROTID ARTERY IN 2965 MEMBERS OF THE FRAMINGHAM OFFSPRING STUDY COHORT. CARDIOVASCULAR-DISEASE OUTCOMES WERE EVALUATED FOR AN AVERAGE FOLLOW-UP OF 7.2 YEARS. MULTIVARIABLE COX PROPORTIONAL-HAZARDS MODEL WERE GENERATED FOR INTIMA-MEDIA THICKNESS AND RISK FACTORS. WE EVALUATED THE RECLASSIFICATION OF CARDIOVASCULAR DISEASE ON THE BASIS OF THE 8-YEAR FRAMINGHAM RISK SCORE CATEGORY (LOW, INTERMEDIATE, OR HIGH) AFTER ADDING INTIMA-MEDIA THICKNESS VALUES.

RESULTS. A TOTAL OF 296 PARTICIPANTS HAD A CARDIOVASCULAR EVENT. THE RISK FACTORS OF THE FRAMINGHAM RISK SCORE PREDICTED THESE EVENTS, WITH A C STATISTIC OF 0.748 (95% CONFIDENCE INTERVAL [CI], 0.719 TO 0.776). THE ADJUSTED HAZARD RATIO FOR CARDIOVASCULAR DISEASE WITH A 1-SD INCREASE IN THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY WAS 1.13 (95% CI, 0.000 TO 0.007): THE CORRESPONDING HAZARD RATIO FOR THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY WAS 1.21 (95% CI, 0.003 TO 0.016). THE NET RECLASSIFICATION INDEX INCREASED SIGNIFICANTLY AFTER ADDITION OF INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY (7.6%, P <0.001) BUT NOT INTIMA. MEDIA THICKNESS OF THE COMMON CAROTID ARTERY (0.0%, P=0.99). WITH THE PRESENCE OF PLAQUE, DEFINED AS INTIMA- MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY OF MORE THAN 1.5 MM, THE NET RECLASSIFICATION INDEX WAS 7.3%
(P-0.01), WITH AN INCREASE IN THE C STATISTIC OF 0.014 (95% CI, 0.003 TO 0.025)

CONCLUSIONS. THE MAXIMUM INTERNAL AND MEAN COMMON CAROTID-ARTERY INTIMA-MEDIA THICKNESSES BOTH PREDICT CARDIOVASCULAR OUTCOMES, BUT ONLY THE MAXIMUM INTIMA-MEDIA THICKNESS OF (AND PRESENCE OF PLAQUE IN) THE INTERNAL CAROTID ARTERY SIGNIFICANTLY (ALBEIT MODESTLY) IMPROVES THE CLASSIFICATION OF RISK OF CARDIOVASCULAR DISEASE IN THE FRAMINGHAM OFFSPRING STUDY COHORT.

THE AIM OF THIS STUDY WAS:
SELECCIONE UNA:

CASO CLÍNICO SERIADO 3/5

CAROTID-WALL INTIMA-MEDIA THICKNESS AND CARDIOVASCULAR EVENTS

JOSEPH F. POLAK, N ENGL J MED 2011; 365:213-221 JULY 21, 2011

BACKGROUND. INTIMA-MEDIA THICKNESS OF THE WALLS OF THE COMMON CAROTID ARTERY AND INTERNAL CAROTID ARTERY MAY ADD TO THE FRAMINGHAM RISK SCORE FOR PREDICTING CARDIOVASCULAR EVENTS.

METHODS. WE MEASURED THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY AND THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNA CAROTID ARTERY IN 2965 MEMBERS OF THE FRAMINGHAM OFFSPRING STUDY COHORT. CARDIOVASCULAR-DISEASE OUTCOMES WERE EVALUATED FOR AN AVERAGE FOLLOW-UP OF 7.2 YEARS. MULTIVARIABLE COX PROPORTIONAL-HAZARDS MODEL WERE GENERATED FOR INTIMA-MEDIA THICKNESS AND RISK FACTORS. WE EVALUATED THE RECLASSIFICATION OF CARDIOVASCULAR DISEASE ON THE BASIS OF THE 8-YEAR FRAMINGHAM RISK SCORE CATEGORY (LOW, INTERMEDIATE, OR HIGH) AFTER ADDING INTIMA-MEDIA THICKNESS VALUES.

RESULTS. A TOTAL OF 296 PARTICIPANTS HAD A CARDIOVASCULAR EVENT. THE RISK FACTORS OF THE FRAMINGHAM RISK SCORE PREDICTED THESE EVENTS, WITH A C STATISTIC OF 0.748 (95% CONFIDENCE INTERVAL [CI], 0.719 TO 0.776). THE ADJUSTED HAZARD RATIO FOR CARDIOVASCULAR DISEASE WITH A 1-SD INCREASE IN THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY WAS 1.13 (95% CI, 0.000 TO 0.007): THE CORRESPONDING HAZARD RATIO FOR THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY WAS 1.21 (95% CI, 0.003 TO 0.016). THE NET RECLASSIFICATION INDEX INCREASED SIGNIFICANTLY AFTER ADDITION OF INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY (7.6%, P <0.001) BUT NOT INTIMA. MEDIA THICKNESS OF THE COMMON CAROTID ARTERY (0.0%, P=0.99). WITH THE PRESENCE OF PLAQUE, DEFINED AS INTIMA- MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY OF MORE THAN 1.5 MM, THE NET RECLASSIFICATION INDEX WAS 7.3%
(P-0.01), WITH AN INCREASE IN THE C STATISTIC OF 0.014 (95% CI, 0.003 TO 0.025)

CONCLUSIONS. THE MAXIMUM INTERNAL AND MEAN COMMON CAROTID-ARTERY INTIMA-MEDIA THICKNESSES BOTH PREDICT CARDIOVASCULAR OUTCOMES, BUT ONLY THE MAXIMUM INTIMA-MEDIA THICKNESS OF (AND PRESENCE OF PLAQUE IN) THE INTERNAL CAROTID ARTERY SIGNIFICANTLY (ALBEIT MODESTLY) IMPROVES THE CLASSIFICATION OF RISK OF CARDIOVASCULAR DISEASE IN THE FRAMINGHAM OFFSPRING STUDY COHORT.

IN WHICH ARTERIES NO WAS SIGNIFICANT CHANGES?
SELECCIONE UNA:

CASO CLÍNICO SERIADO 4/5

CAROTID-WALL INTIMA-MEDIA THICKNESS AND CARDIOVASCULAR EVENTS

JOSEPH F. POLAK, N ENGL J MED 2011; 365:213-221 JULY 21, 2011

BACKGROUND. INTIMA-MEDIA THICKNESS OF THE WALLS OF THE COMMON CAROTID ARTERY AND INTERNAL CAROTID ARTERY MAY ADD TO THE FRAMINGHAM RISK SCORE FOR PREDICTING CARDIOVASCULAR EVENTS.

METHODS. WE MEASURED THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY AND THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNA CAROTID ARTERY IN 2965 MEMBERS OF THE FRAMINGHAM OFFSPRING STUDY COHORT. CARDIOVASCULAR-DISEASE OUTCOMES WERE EVALUATED FOR AN AVERAGE FOLLOW-UP OF 7.2 YEARS. MULTIVARIABLE COX PROPORTIONAL-HAZARDS MODEL WERE GENERATED FOR INTIMA-MEDIA THICKNESS AND RISK FACTORS. WE EVALUATED THE RECLASSIFICATION OF CARDIOVASCULAR DISEASE ON THE BASIS OF THE 8-YEAR FRAMINGHAM RISK SCORE CATEGORY (LOW, INTERMEDIATE, OR HIGH) AFTER ADDING INTIMA-MEDIA THICKNESS VALUES.

RESULTS. A TOTAL OF 296 PARTICIPANTS HAD A CARDIOVASCULAR EVENT. THE RISK FACTORS OF THE FRAMINGHAM RISK SCORE PREDICTED THESE EVENTS, WITH A C STATISTIC OF 0.748 (95% CONFIDENCE INTERVAL [CI], 0.719 TO 0.776). THE ADJUSTED HAZARD RATIO FOR CARDIOVASCULAR DISEASE WITH A 1-SD INCREASE IN THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY WAS 1.13 (95% CI, 0.000 TO 0.007): THE CORRESPONDING HAZARD RATIO FOR THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY WAS 1.21 (95% CI, 0.003 TO 0.016). THE NET RECLASSIFICATION INDEX INCREASED SIGNIFICANTLY AFTER ADDITION OF INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY (7.6%, P <0.001) BUT NOT INTIMA. MEDIA THICKNESS OF THE COMMON CAROTID ARTERY (0.0%, P=0.99). WITH THE PRESENCE OF PLAQUE, DEFINED AS INTIMA- MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY OF MORE THAN 1.5 MM, THE NET RECLASSIFICATION INDEX WAS 7.3%
(P-0.01), WITH AN INCREASE IN THE C STATISTIC OF 0.014 (95% CI, 0.003 TO 0.025)

CONCLUSIONS. THE MAXIMUM INTERNAL AND MEAN COMMON CAROTID-ARTERY INTIMA-MEDIA THICKNESSES BOTH PREDICT CARDIOVASCULAR OUTCOMES, BUT ONLY THE MAXIMUM INTIMA-MEDIA THICKNESS OF (AND PRESENCE OF PLAQUE IN) THE INTERNAL CAROTID ARTERY SIGNIFICANTLY (ALBEIT MODESTLY) IMPROVES THE CLASSIFICATION OF RISK OF CARDIOVASCULAR DISEASE IN THE FRAMINGHAM OFFSPRING STUDY COHORT.

THAT PARAMETER SHOULD BE ADDED TO CARDIOVASCULAR RISK
SELECCIONE UNA:

CASO CLÍNICO SERIADO 5/5

CAROTID-WALL INTIMA-MEDIA THICKNESS AND CARDIOVASCULAR EVENTS

JOSEPH F. POLAK, N ENGL J MED 2011; 365:213-221 JULY 21, 2011

BACKGROUND. INTIMA-MEDIA THICKNESS OF THE WALLS OF THE COMMON CAROTID ARTERY AND INTERNAL CAROTID ARTERY MAY ADD TO THE FRAMINGHAM RISK SCORE FOR PREDICTING CARDIOVASCULAR EVENTS.

METHODS. WE MEASURED THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY AND THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNA CAROTID ARTERY IN 2965 MEMBERS OF THE FRAMINGHAM OFFSPRING STUDY COHORT. CARDIOVASCULAR-DISEASE OUTCOMES WERE EVALUATED FOR AN AVERAGE FOLLOW-UP OF 7.2 YEARS. MULTIVARIABLE COX PROPORTIONAL-HAZARDS MODEL WERE GENERATED FOR INTIMA-MEDIA THICKNESS AND RISK FACTORS. WE EVALUATED THE RECLASSIFICATION OF CARDIOVASCULAR DISEASE ON THE BASIS OF THE 8-YEAR FRAMINGHAM RISK SCORE CATEGORY (LOW, INTERMEDIATE, OR HIGH) AFTER ADDING INTIMA-MEDIA THICKNESS VALUES.

RESULTS. A TOTAL OF 296 PARTICIPANTS HAD A CARDIOVASCULAR EVENT. THE RISK FACTORS OF THE FRAMINGHAM RISK SCORE PREDICTED THESE EVENTS, WITH A C STATISTIC OF 0.748 (95% CONFIDENCE INTERVAL [CI], 0.719 TO 0.776). THE ADJUSTED HAZARD RATIO FOR CARDIOVASCULAR DISEASE WITH A 1-SD INCREASE IN THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY WAS 1.13 (95% CI, 0.000 TO 0.007): THE CORRESPONDING HAZARD RATIO FOR THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY WAS 1.21 (95% CI, 0.003 TO 0.016). THE NET RECLASSIFICATION INDEX INCREASED SIGNIFICANTLY AFTER ADDITION OF INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY (7.6%, P <0.001) BUT NOT INTIMA. MEDIA THICKNESS OF THE COMMON CAROTID ARTERY (0.0%, P=0.99). WITH THE PRESENCE OF PLAQUE, DEFINED AS INTIMA- MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY OF MORE THAN 1.5 MM, THE NET RECLASSIFICATION INDEX WAS 7.3%
(P-0.01), WITH AN INCREASE IN THE C STATISTIC OF 0.014 (95% CI, 0.003 TO 0.025)

CONCLUSIONS. THE MAXIMUM INTERNAL AND MEAN COMMON CAROTID-ARTERY INTIMA-MEDIA THICKNESSES BOTH PREDICT CARDIOVASCULAR OUTCOMES, BUT ONLY THE MAXIMUM INTIMA-MEDIA THICKNESS OF (AND PRESENCE OF PLAQUE IN) THE INTERNAL CAROTID ARTERY SIGNIFICANTLY (ALBEIT MODESTLY) IMPROVES THE CLASSIFICATION OF RISK OF CARDIOVASCULAR DISEASE IN THE FRAMINGHAM OFFSPRING STUDY COHORT.

RECLASSIFIED AS CARDIOVASCULAR RISK WITH A P> 0.01 (WITH CONFIDENCE INTERVAL 95% 0.003-0.025) THIS INTERVAL SHOULD
BE INTERPRETED AS:
SELECCIONE UNA:

CASO CLÍNICO SERIADO 1/5

CAROTID-WALL INTIMA-MEDIA THICKNESS AND CARDIOVASCULAR EVENTS

JOSEPH F. POLAK, N ENGL J MED 2011; 365:213-221 JULY 21, 2011

BACKGROUND. INTIMA-MEDIA THICKNESS OF THE WALLS OF THE COMMON CAROTID ARTERY AND INTERNAL CAROTID ARTERY MAY ADD TO THE FRAMINGHAM RISK SCORE FOR PREDICTING CARDIOVASCULAR EVENTS.

METHODS. WE MEASURED THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY AND THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNA CAROTID ARTERY IN 2965 MEMBERS OF THE FRAMINGHAM OFFSPRING STUDY COHORT. CARDIOVASCULAR-DISEASE OUTCOMES WERE EVALUATED FOR AN AVERAGE FOLLOW-UP OF 7.2 YEARS. MULTIVARIABLE COX PROPORTIONAL-HAZARDS MODEL WERE GENERATED FOR INTIMA-MEDIA THICKNESS AND RISK FACTORS. WE EVALUATED THE RECLASSIFICATION OF CARDIOVASCULAR DISEASE ON THE BASIS OF THE 8-YEAR FRAMINGHAM RISK SCORE CATEGORY (LOW, INTERMEDIATE, OR HIGH) AFTER ADDING INTIMA-MEDIA THICKNESS VALUES.

RESULTS. A TOTAL OF 296 PARTICIPANTS HAD A CARDIOVASCULAR EVENT. THE RISK FACTORS OF THE FRAMINGHAM RISK SCORE PREDICTED THESE EVENTS, WITH A C STATISTIC OF 0.748 (95% CONFIDENCE INTERVAL [CI], 0.719 TO 0.776). THE ADJUSTED HAZARD RATIO FOR CARDIOVASCULAR DISEASE WITH A 1-SD INCREASE IN THE MEAN INTIMA-MEDIA THICKNESS OF THE COMMON CAROTID ARTERY WAS 1.13 (95% CI, 0.000 TO 0.007): THE CORRESPONDING HAZARD RATIO FOR THE MAXIMUM INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY WAS 1.21 (95% CI, 0.003 TO 0.016). THE NET RECLASSIFICATION INDEX INCREASED SIGNIFICANTLY AFTER ADDITION OF INTIMA-MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY (7.6%, P <0.001) BUT NOT INTIMA. MEDIA THICKNESS OF THE COMMON CAROTID ARTERY (0.0%, P=0.99). WITH THE PRESENCE OF PLAQUE, DEFINED AS INTIMA- MEDIA THICKNESS OF THE INTERNAL CAROTID ARTERY OF MORE THAN 1.5 MM, THE NET RECLASSIFICATION INDEX WAS 7.3%
(P-0.01), WITH AN INCREASE IN THE C STATISTIC OF 0.014 (95% CI, 0.003 TO 0.025)

CONCLUSIONS. THE MAXIMUM INTERNAL AND MEAN COMMON CAROTID-ARTERY INTIMA-MEDIA THICKNESSES BOTH PREDICT CARDIOVASCULAR OUTCOMES, BUT ONLY THE MAXIMUM INTIMA-MEDIA THICKNESS OF (AND PRESENCE OF PLAQUE IN) THE INTERNAL CAROTID ARTERY SIGNIFICANTLY (ALBEIT MODESTLY) IMPROVES THE CLASSIFICATION OF RISK OF CARDIOVASCULAR DISEASE IN THE FRAMINGHAM OFFSPRING STUDY COHORT.
COHORT STUDIES ARE ALSO DESCRIBED AS:

SELECCIONE UNA:

CASO CLÍNICO SERIADO 2/5

FEBRILE URINARY TRACT INFECTIONS IN CHILDREN
GIOVANNI MONTINI, N ENGL J MED 2011; 365:239-250
ACUTE PYELONEPHRITIS IS THE MOST COMMON SERIOUS BACTERIAL INFECTION IN CHILDHOOD; MANY AFFECTED CHILDREN, PARTICULARLY INFANTS, HAVE SEVERE SYMPTOMS. MOST CASES ARE READILY TREATED, PROVIDED DIAGNOSIS IS PROMPT, THOUGH IN SOME CHILDREN FEVER MAY TAKE SEVERAL DAYS TO ABATE. APPROXIMATELY 7 TO 8% OF GIRLS AND 2% OF BOYS HAVE A URINARY TRACT INFECTION DURING THE FIRST 8 YEARS OF LIFE. FEBRILE URINARY TRACT INFECTIONS HAVE THE HIGHEST INCIDENCE DURING THE FIRST YEAR OF LIFE IN BOTH SEXES, WHEREAS NONFEBRILE URINARY TRACT INFECTIONS OCCUR PREDOMINANTLY IN GIRLS OLDER THAN 3 YEARS. AFTER INFANCY, URINARY TRACT INFECTIONS CONFINED TO THE BLADDER ARE GENERALLY ACCOMPANIED BY LOCALIZED SYMPTOMS AND ARE EASILY TREATED. IN CONTRAST, THE PRESENCE OF FEVER INCREASES THE PROBABILITY OF KIDNEY INVOLVEMENT (SENSITIVITY, 53 TO 84%; SPECIFICITY, 44 TO 92%) AND IS ASSOCIATED WITH AN INCREASED LIKELIHOOD OF UNDERLYING NEPHROUROLOGIC ABNORMALITIES AND A GREATER RISK OF CONSEQUENT RENAL SCARRING. KIDNEY SCARRING RELATED TO URINARY TRACT INFECTIONS HAS BEEN CONSIDERED A CAUSE OF SUBSTANCIAL LON-TERM MORBIDITY. THUS, CHILDREN WITH PROVEN INFECTIONS HAVE BEEN INTENSIVELY EVALUATED AND TREATED, AND THEY HAVE OFTEN UNDERGONE SURGERY OR HAVE RECEIVED LONG-TERM ANTIBIOTIC PROPHYLAXIS. SUCH APPROACHES HAVE BEEN QUESTIONS. A NUMBER OF TRIALS HAVE BEEN CONDUCTED OR ARE UNDER WAY TO DETERMINE OPTIMAL APPROACHES TO THE ASSESSMENT AND MANAGEMENT OF INITIAL FEBRILE URINARY TRACT INFECTIONS AND SUBSEQUENT INTERVENTIONS FOR THEM.

LONG TERM CONSEQUENCES
APPROXIMATELY 60% OF CHILDREN WITH FEBRILE URINARY TRACT INFECTIONS, IF EVALUATED DURING OR JUST AFTER THE INFECTION, HAVE VISIBLE PHOTON DEFECTS ON RENAL SCINTIGRAPHIC STUDIES WITH TECHNETIUM-99M-LABELED DIMERCAPTOSUCCINIC ACID (DMSA)-FINDINGS CONSIDERED EVIDENCE OF PARENCHYMAL LOCALIZATION (PYELONEPHRITIS). OF THESE, 1 0 TO 40% WILL HAVE PERMANENT RENAL SCARRING, UNRELATED TO AGE. THE LONG-TERM MEDICAL RISK OF INFECTION-RELATED SCARRING IN PREVIOUSLY HEALTHY KIDNEYS ARE INCOMPLETELY UNDERSTOOD. FEW POPULATION-BASED, FOLLOW-UP STUDIES HAVE BEEN PERFORMED. A SWEDISH STUDY FOLLOWED 57 CHILDREN WITH NONOBSTRUCTIVE RENAL SCARRING AND 51 MATCHED SUBJECTS WITHOUT RENALSCARRING AT UROGRAPHIC EXAMINATION, 16 TO 26 YEARS AFTER  A FIRST SYMPTOMATIC URINARY TRACT INFECTION. CHILDREN WITH UNILATERAL SCARS AND THOSE WITHOUT SCARS HAD SIMILAR GLOMERULAR FILTRATION RATES AT THE END OF FOLLOW-UP; HOWEVER, THE MEDIAN GLOMERULAR FILTRATION RATE IN SEVEN CHILDREN WITH BILATERAL SCARS DECREASES FROM 94 ML PER MINUTE PEER 1.73 M2 OF BODY-SURFACE AREA TO 84 ML PER MINUTE PER 1.73M2. NO DIFFERENCE IN AMBULATORY 24-HOUR BLOOD PRESSURE WAS FOUND BETWEEN CHILDREN WITH SCARS AND THOSE WITHOUT SCARS. THE FEW PROSPECTIVE STUDIES THAT HAVE BEEN PERFORMED SHOWED A LOW RATE OF LONG-TERM CONSEQUENCES. IN THE INTERNATIONAL REFLUX STUDY IN CHILDREN HYPERTENSION WAS REPORTED IN 4 OF 252 PATIENTS (1.6%) WITH REFLUX, MAINLY GRADE IV, PROSPECTIVELY FOLLOWED FOR 10 YEARS. (THE CLASSIFICATION OF VESICOURETERAL REFLUX IS EXPLAINED IN). ONE OF THE 133 CHILDREN WHOSE GLOMERULAR FILTRATION RATE WAS MEASURED HAD A CLEARANCE THAT HAD FALLEN BELOW THE MINIMAL STUDY ENTRY LEVEL OF 70 ML PER MINUTE PER 1.73M2 .30 MOST OF THE PROSPECTIVE STUDIES ARE LIMITED BY RELATIVELY SHORT FOLLOW-UP. IN CONTRAST, RETROSPECTIVE STUDIES HAVE SUGGESTED THAT RENAL SCARRING RELATED TO URINARY TRACT INFECTION CARRIES A CLINICALLY SIGNIFICANT RISK, WITH HIGH SUBSEQUENT RATES OF CHRONIC KIDNEY DISEASE (UP TO 20%), HYPERTENSION (20% TO 40%), AND PREECLAMPSIA (10 TO 20%). SUCH RETROSPECTIVE STUDIES ARE LIMITED BY REFERRAL BIAS IN THAT SPECIALIZED CENTERS MAY NOT SEE THE VAST MAJORITY OF CHILDREN, WHO HAVE UNCOMPLICATED FEBRILE URINARY TRACT INFECTIONS. IN ADDITION, SOME RETROSPECTIVE STUDIES RECRUITED PATIENTS BEFORE THE WIDESPREAD AVAILABILITY OF PRENATAL ULTRASONOGRAPHIC SCREENING. FURTHERMORE, OTHER STUDIES ASSUMED THAT ALL PATIENT WITH CHRONIC KIDNEY DISEASE AND VESICOURETERAL REFLUX HAD HAD UNDOCUMENTED URINARY TRACT INFECTIONS IN THE PAST.
ASYMPTOMATIC URINARY INFECTIONS ARE MORE COMMON IN GIRLS AT WHAT AGE.

THE FEVER INCREASES THE RISK OF URINARY INFECTION IN
SELECCIONE UNA:

CASO CLÍNICO SERIADO 3/5

FEBRILE URINARY TRACT INFECTIONS IN CHILDREN
GIOVANNI MONTINI, N ENGL J MED 2011; 365:239-250
ACUTE PYELONEPHRITIS IS THE MOST COMMON SERIOUS BACTERIAL INFECTION IN CHILDHOOD; MANY AFFECTED CHILDREN, PARTICULARLY INFANTS, HAVE SEVERE SYMPTOMS. MOST CASES ARE READILY TREATED, PROVIDED DIAGNOSIS IS PROMPT, THOUGH IN SOME CHILDREN FEVER MAY TAKE SEVERAL DAYS TO ABATE. APPROXIMATELY 7 TO 8% OF GIRLS AND 2% OF BOYS HAVE A URINARY TRACT INFECTION DURING THE FIRST 8 YEARS OF LIFE. FEBRILE URINARY TRACT INFECTIONS HAVE THE HIGHEST INCIDENCE DURING THE FIRST YEAR OF LIFE IN BOTH SEXES, WHEREAS NONFEBRILE URINARY TRACT INFECTIONS OCCUR PREDOMINANTLY IN GIRLS OLDER THAN 3 YEARS. AFTER INFANCY, URINARY TRACT INFECTIONS CONFINED TO THE BLADDER ARE GENERALLY ACCOMPANIED BY LOCALIZED SYMPTOMS AND ARE EASILY TREATED. IN CONTRAST, THE PRESENCE OF FEVER INCREASES THE PROBABILITY OF KIDNEY INVOLVEMENT (SENSITIVITY, 53 TO 84%; SPECIFICITY, 44 TO 92%) AND IS ASSOCIATED WITH AN INCREASED LIKELIHOOD OF UNDERLYING NEPHROUROLOGIC ABNORMALITIES AND A GREATER RISK OF CONSEQUENT RENAL SCARRING. KIDNEY SCARRING RELATED TO URINARY TRACT INFECTIONS HAS BEEN CONSIDERED A CAUSE OF SUBSTANCIAL LON-TERM MORBIDITY. THUS, CHILDREN WITH PROVEN INFECTIONS HAVE BEEN INTENSIVELY EVALUATED AND TREATED, AND THEY HAVE OFTEN UNDERGONE SURGERY OR HAVE RECEIVED LONG-TERM ANTIBIOTIC PROPHYLAXIS. SUCH APPROACHES HAVE BEEN QUESTIONS. A NUMBER OF TRIALS HAVE BEEN CONDUCTED OR ARE UNDER WAY TO DETERMINE OPTIMAL APPROACHES TO THE ASSESSMENT AND MANAGEMENT OF INITIAL FEBRILE URINARY TRACT INFECTIONS AND SUBSEQUENT INTERVENTIONS FOR THEM.

LONG TERM CONSEQUENCES
APPROXIMATELY 60% OF CHILDREN WITH FEBRILE URINARY TRACT INFECTIONS, IF EVALUATED DURING OR JUST AFTER THE INFECTION, HAVE VISIBLE PHOTON DEFECTS ON RENAL SCINTIGRAPHIC STUDIES WITH TECHNETIUM-99M-LABELED DIMERCAPTOSUCCINIC ACID (DMSA)-FINDINGS CONSIDERED EVIDENCE OF PARENCHYMAL LOCALIZATION (PYELONEPHRITIS). OF THESE, 1 0 TO 40% WILL HAVE PERMANENT RENAL SCARRING, UNRELATED TO AGE. THE LONG-TERM MEDICAL RISK OF INFECTION-RELATED SCARRING IN PREVIOUSLY HEALTHY KIDNEYS ARE INCOMPLETELY UNDERSTOOD. FEW POPULATION-BASED, FOLLOW-UP STUDIES HAVE BEEN PERFORMED. A SWEDISH STUDY FOLLOWED 57 CHILDREN WITH NONOBSTRUCTIVE RENAL SCARRING AND 51 MATCHED SUBJECTS WITHOUT RENALSCARRING AT UROGRAPHIC EXAMINATION, 16 TO 26 YEARS AFTER  A FIRST SYMPTOMATIC URINARY TRACT INFECTION. CHILDREN WITH UNILATERAL SCARS AND THOSE WITHOUT SCARS HAD SIMILAR GLOMERULAR FILTRATION RATES AT THE END OF FOLLOW-UP; HOWEVER, THE MEDIAN GLOMERULAR FILTRATION RATE IN SEVEN CHILDREN WITH BILATERAL SCARS DECREASES FROM 94 ML PER MINUTE PEER 1.73 M2 OF BODY-SURFACE AREA TO 84 ML PER MINUTE PER 1.73M2. NO DIFFERENCE IN AMBULATORY 24-HOUR BLOOD PRESSURE WAS FOUND BETWEEN CHILDREN WITH SCARS AND THOSE WITHOUT SCARS. THE FEW PROSPECTIVE STUDIES THAT HAVE BEEN PERFORMED SHOWED A LOW RATE OF LONG-TERM CONSEQUENCES. IN THE INTERNATIONAL REFLUX STUDY IN CHILDREN HYPERTENSION WAS REPORTED IN 4 OF 252 PATIENTS (1.6%) WITH REFLUX, MAINLY GRADE IV, PROSPECTIVELY FOLLOWED FOR 10 YEARS. (THE CLASSIFICATION OF VESICOURETERAL REFLUX IS EXPLAINED IN). ONE OF THE 133 CHILDREN WHOSE GLOMERULAR FILTRATION RATE WAS MEASURED HAD A CLEARANCE THAT HAD FALLEN BELOW THE MINIMAL STUDY ENTRY LEVEL OF 70 ML PER MINUTE PER 1.73M2 .30 MOST OF THE PROSPECTIVE STUDIES ARE LIMITED BY RELATIVELY SHORT FOLLOW-UP. IN CONTRAST, RETROSPECTIVE STUDIES HAVE SUGGESTED THAT RENAL SCARRING RELATED TO URINARY TRACT INFECTION CARRIES A CLINICALLY SIGNIFICANT RISK, WITH HIGH SUBSEQUENT RATES OF CHRONIC KIDNEY DISEASE (UP TO 20%), HYPERTENSION (20% TO 40%), AND PREECLAMPSIA (10 TO 20%). SUCH RETROSPECTIVE STUDIES ARE LIMITED BY REFERRAL BIAS IN THAT SPECIALIZED CENTERS MAY NOT SEE THE VAST MAJORITY OF CHILDREN, WHO HAVE UNCOMPLICATED FEBRILE URINARY TRACT INFECTIONS. IN ADDITION, SOME RETROSPECTIVE STUDIES RECRUITED PATIENTS BEFORE THE WIDESPREAD AVAILABILITY OF PRENATAL ULTRASONOGRAPHIC SCREENING. FURTHERMORE, OTHER STUDIES ASSUMED THAT ALL PATIENT WITH CHRONIC KIDNEY DISEASE AND VESICOURETERAL REFLUX HAD HAD UNDOCUMENTED URINARY TRACT INFECTIONS IN THE PAST.
ASYMPTOMATIC URINARY INFECTIONS ARE MORE COMMON IN GIRLS AT WHAT AGE.

SWEDISH TYPE OF STUDY THAT IS DISCUSSED BY THE AUTHOR?
SELECCIONE UNA:

CASO CLÍNICO SERIADO 4/5

FEBRILE URINARY TRACT INFECTIONS IN CHILDREN
GIOVANNI MONTINI, N ENGL J MED 2011; 365:239-250
ACUTE PYELONEPHRITIS IS THE MOST COMMON SERIOUS BACTERIAL INFECTION IN CHILDHOOD; MANY AFFECTED CHILDREN, PARTICULARLY INFANTS, HAVE SEVERE SYMPTOMS. MOST CASES ARE READILY TREATED, PROVIDED DIAGNOSIS IS PROMPT, THOUGH IN SOME CHILDREN FEVER MAY TAKE SEVERAL DAYS TO ABATE. APPROXIMATELY 7 TO 8% OF GIRLS AND 2% OF BOYS HAVE A URINARY TRACT INFECTION DURING THE FIRST 8 YEARS OF LIFE. FEBRILE URINARY TRACT INFECTIONS HAVE THE HIGHEST INCIDENCE DURING THE FIRST YEAR OF LIFE IN BOTH SEXES, WHEREAS NONFEBRILE URINARY TRACT INFECTIONS OCCUR PREDOMINANTLY IN GIRLS OLDER THAN 3 YEARS. AFTER INFANCY, URINARY TRACT INFECTIONS CONFINED TO THE BLADDER ARE GENERALLY ACCOMPANIED BY LOCALIZED SYMPTOMS AND ARE EASILY TREATED. IN CONTRAST, THE PRESENCE OF FEVER INCREASES THE PROBABILITY OF KIDNEY INVOLVEMENT (SENSITIVITY, 53 TO 84%; SPECIFICITY, 44 TO 92%) AND IS ASSOCIATED WITH AN INCREASED LIKELIHOOD OF UNDERLYING NEPHROUROLOGIC ABNORMALITIES AND A GREATER RISK OF CONSEQUENT RENAL SCARRING. KIDNEY SCARRING RELATED TO URINARY TRACT INFECTIONS HAS BEEN CONSIDERED A CAUSE OF SUBSTANCIAL LON-TERM MORBIDITY. THUS, CHILDREN WITH PROVEN INFECTIONS HAVE BEEN INTENSIVELY EVALUATED AND TREATED, AND THEY HAVE OFTEN UNDERGONE SURGERY OR HAVE RECEIVED LONG-TERM ANTIBIOTIC PROPHYLAXIS. SUCH APPROACHES HAVE BEEN QUESTIONS. A NUMBER OF TRIALS HAVE BEEN CONDUCTED OR ARE UNDER WAY TO DETERMINE OPTIMAL APPROACHES TO THE ASSESSMENT AND MANAGEMENT OF INITIAL FEBRILE URINARY TRACT INFECTIONS AND SUBSEQUENT INTERVENTIONS FOR THEM.

LONG TERM CONSEQUENCES
APPROXIMATELY 60% OF CHILDREN WITH FEBRILE URINARY TRACT INFECTIONS, IF EVALUATED DURING OR JUST AFTER THE INFECTION, HAVE VISIBLE PHOTON DEFECTS ON RENAL SCINTIGRAPHIC STUDIES WITH TECHNETIUM-99M-LABELED DIMERCAPTOSUCCINIC ACID (DMSA)-FINDINGS CONSIDERED EVIDENCE OF PARENCHYMAL LOCALIZATION (PYELONEPHRITIS). OF THESE, 1 0 TO 40% WILL HAVE PERMANENT RENAL SCARRING, UNRELATED TO AGE. THE LONG-TERM MEDICAL RISK OF INFECTION-RELATED SCARRING IN PREVIOUSLY HEALTHY KIDNEYS ARE INCOMPLETELY UNDERSTOOD. FEW POPULATION-BASED, FOLLOW-UP STUDIES HAVE BEEN PERFORMED. A SWEDISH STUDY FOLLOWED 57 CHILDREN WITH NONOBSTRUCTIVE RENAL SCARRING AND 51 MATCHED SUBJECTS WITHOUT RENALSCARRING AT UROGRAPHIC EXAMINATION, 16 TO 26 YEARS AFTER  A FIRST SYMPTOMATIC URINARY TRACT INFECTION. CHILDREN WITH UNILATERAL SCARS AND THOSE WITHOUT SCARS HAD SIMILAR GLOMERULAR FILTRATION RATES AT THE END OF FOLLOW-UP; HOWEVER, THE MEDIAN GLOMERULAR FILTRATION RATE IN SEVEN CHILDREN WITH BILATERAL SCARS DECREASES FROM 94 ML PER MINUTE PEER 1.73 M2 OF BODY-SURFACE AREA TO 84 ML PER MINUTE PER 1.73M2. NO DIFFERENCE IN AMBULATORY 24-HOUR BLOOD PRESSURE WAS FOUND BETWEEN CHILDREN WITH SCARS AND THOSE WITHOUT SCARS. THE FEW PROSPECTIVE STUDIES THAT HAVE BEEN PERFORMED SHOWED A LOW RATE OF LONG-TERM CONSEQUENCES. IN THE INTERNATIONAL REFLUX STUDY IN CHILDREN HYPERTENSION WAS REPORTED IN 4 OF 252 PATIENTS (1.6%) WITH REFLUX, MAINLY GRADE IV, PROSPECTIVELY FOLLOWED FOR 10 YEARS. (THE CLASSIFICATION OF VESICOURETERAL REFLUX IS EXPLAINED IN). ONE OF THE 133 CHILDREN WHOSE GLOMERULAR FILTRATION RATE WAS MEASURED HAD A CLEARANCE THAT HAD FALLEN BELOW THE MINIMAL STUDY ENTRY LEVEL OF 70 ML PER MINUTE PER 1.73M2 .30 MOST OF THE PROSPECTIVE STUDIES ARE LIMITED BY RELATIVELY SHORT FOLLOW-UP. IN CONTRAST, RETROSPECTIVE STUDIES HAVE SUGGESTED THAT RENAL SCARRING RELATED TO URINARY TRACT INFECTION CARRIES A CLINICALLY SIGNIFICANT RISK, WITH HIGH SUBSEQUENT RATES OF CHRONIC KIDNEY DISEASE (UP TO 20%), HYPERTENSION (20% TO 40%), AND PREECLAMPSIA (10 TO 20%). SUCH RETROSPECTIVE STUDIES ARE LIMITED BY REFERRAL BIAS IN THAT SPECIALIZED CENTERS MAY NOT SEE THE VAST MAJORITY OF CHILDREN, WHO HAVE UNCOMPLICATED FEBRILE URINARY TRACT INFECTIONS. IN ADDITION, SOME RETROSPECTIVE STUDIES RECRUITED PATIENTS BEFORE THE WIDESPREAD AVAILABILITY OF PRENATAL ULTRASONOGRAPHIC SCREENING. FURTHERMORE, OTHER STUDIES ASSUMED THAT ALL PATIENT WITH CHRONIC KIDNEY DISEASE AND VESICOURETERAL REFLUX HAD HAD UNDOCUMENTED URINARY TRACT INFECTIONS IN THE PAST.
ASYMPTOMATIC URINARY INFECTIONS ARE MORE COMMON IN GIRLS AT WHAT AGE.

WHAT ARE THE LIMITATIONS OF PROSPECTIVE STUDIES DISCUSSED IN THE REVIEW
SELECCIONE UNA:

CASO CLÍNICO SERIADO 5/5

FEBRILE URINARY TRACT INFECTIONS IN CHILDREN
GIOVANNI MONTINI, N ENGL J MED 2011; 365:239-250
ACUTE PYELONEPHRITIS IS THE MOST COMMON SERIOUS BACTERIAL INFECTION IN CHILDHOOD; MANY AFFECTED CHILDREN, PARTICULARLY INFANTS, HAVE SEVERE SYMPTOMS. MOST CASES ARE READILY TREATED, PROVIDED DIAGNOSIS IS PROMPT, THOUGH IN SOME CHILDREN FEVER MAY TAKE SEVERAL DAYS TO ABATE. APPROXIMATELY 7 TO 8% OF GIRLS AND 2% OF BOYS HAVE A URINARY TRACT INFECTION DURING THE FIRST 8 YEARS OF LIFE. FEBRILE URINARY TRACT INFECTIONS HAVE THE HIGHEST INCIDENCE DURING THE FIRST YEAR OF LIFE IN BOTH SEXES, WHEREAS NONFEBRILE URINARY TRACT INFECTIONS OCCUR PREDOMINANTLY IN GIRLS OLDER THAN 3 YEARS. AFTER INFANCY, URINARY TRACT INFECTIONS CONFINED TO THE BLADDER ARE GENERALLY ACCOMPANIED BY LOCALIZED SYMPTOMS AND ARE EASILY TREATED. IN CONTRAST, THE PRESENCE OF FEVER INCREASES THE PROBABILITY OF KIDNEY INVOLVEMENT (SENSITIVITY, 53 TO 84%; SPECIFICITY, 44 TO 92%) AND IS ASSOCIATED WITH AN INCREASED LIKELIHOOD OF UNDERLYING NEPHROUROLOGIC ABNORMALITIES AND A GREATER RISK OF CONSEQUENT RENAL SCARRING. KIDNEY SCARRING RELATED TO URINARY TRACT INFECTIONS HAS BEEN CONSIDERED A CAUSE OF SUBSTANCIAL LON-TERM MORBIDITY. THUS, CHILDREN WITH PROVEN INFECTIONS HAVE BEEN INTENSIVELY EVALUATED AND TREATED, AND THEY HAVE OFTEN UNDERGONE SURGERY OR HAVE RECEIVED LONG-TERM ANTIBIOTIC PROPHYLAXIS. SUCH APPROACHES HAVE BEEN QUESTIONS. A NUMBER OF TRIALS HAVE BEEN CONDUCTED OR ARE UNDER WAY TO DETERMINE OPTIMAL APPROACHES TO THE ASSESSMENT AND MANAGEMENT OF INITIAL FEBRILE URINARY TRACT INFECTIONS AND SUBSEQUENT INTERVENTIONS FOR THEM.

LONG TERM CONSEQUENCES
APPROXIMATELY 60% OF CHILDREN WITH FEBRILE URINARY TRACT INFECTIONS, IF EVALUATED DURING OR JUST AFTER THE INFECTION, HAVE VISIBLE PHOTON DEFECTS ON RENAL SCINTIGRAPHIC STUDIES WITH TECHNETIUM-99M-LABELED DIMERCAPTOSUCCINIC ACID (DMSA)-FINDINGS CONSIDERED EVIDENCE OF PARENCHYMAL LOCALIZATION (PYELONEPHRITIS). OF THESE, 1 0 TO 40% WILL HAVE PERMANENT RENAL SCARRING, UNRELATED TO AGE. THE LONG-TERM MEDICAL RISK OF INFECTION-RELATED SCARRING IN PREVIOUSLY HEALTHY KIDNEYS ARE INCOMPLETELY UNDERSTOOD. FEW POPULATION-BASED, FOLLOW-UP STUDIES HAVE BEEN PERFORMED. A SWEDISH STUDY FOLLOWED 57 CHILDREN WITH NONOBSTRUCTIVE RENAL SCARRING AND 51 MATCHED SUBJECTS WITHOUT RENALSCARRING AT UROGRAPHIC EXAMINATION, 16 TO 26 YEARS AFTER  A FIRST SYMPTOMATIC URINARY TRACT INFECTION. CHILDREN WITH UNILATERAL SCARS AND THOSE WITHOUT SCARS HAD SIMILAR GLOMERULAR FILTRATION RATES AT THE END OF FOLLOW-UP; HOWEVER, THE MEDIAN GLOMERULAR FILTRATION RATE IN SEVEN CHILDREN WITH BILATERAL SCARS DECREASES FROM 94 ML PER MINUTE PEER 1.73 M2 OF BODY-SURFACE AREA TO 84 ML PER MINUTE PER 1.73M2. NO DIFFERENCE IN AMBULATORY 24-HOUR BLOOD PRESSURE WAS FOUND BETWEEN CHILDREN WITH SCARS AND THOSE WITHOUT SCARS. THE FEW PROSPECTIVE STUDIES THAT HAVE BEEN PERFORMED SHOWED A LOW RATE OF LONG-TERM CONSEQUENCES. IN THE INTERNATIONAL REFLUX STUDY IN CHILDREN HYPERTENSION WAS REPORTED IN 4 OF 252 PATIENTS (1.6%) WITH REFLUX, MAINLY GRADE IV, PROSPECTIVELY FOLLOWED FOR 10 YEARS. (THE CLASSIFICATION OF VESICOURETERAL REFLUX IS EXPLAINED IN). ONE OF THE 133 CHILDREN WHOSE GLOMERULAR FILTRATION RATE WAS MEASURED HAD A CLEARANCE THAT HAD FALLEN BELOW THE MINIMAL STUDY ENTRY LEVEL OF 70 ML PER MINUTE PER 1.73M2 .30 MOST OF THE PROSPECTIVE STUDIES ARE LIMITED BY RELATIVELY SHORT FOLLOW-UP. IN CONTRAST, RETROSPECTIVE STUDIES HAVE SUGGESTED THAT RENAL SCARRING RELATED TO URINARY TRACT INFECTION CARRIES A CLINICALLY SIGNIFICANT RISK, WITH HIGH SUBSEQUENT RATES OF CHRONIC KIDNEY DISEASE (UP TO 20%), HYPERTENSION (20% TO 40%), AND PREECLAMPSIA (10 TO 20%). SUCH RETROSPECTIVE STUDIES ARE LIMITED BY REFERRAL BIAS IN THAT SPECIALIZED CENTERS MAY NOT SEE THE VAST MAJORITY OF CHILDREN, WHO HAVE UNCOMPLICATED FEBRILE URINARY TRACT INFECTIONS. IN ADDITION, SOME RETROSPECTIVE STUDIES RECRUITED PATIENTS BEFORE THE WIDESPREAD AVAILABILITY OF PRENATAL ULTRASONOGRAPHIC SCREENING. FURTHERMORE, OTHER STUDIES ASSUMED THAT ALL PATIENT WITH CHRONIC KIDNEY DISEASE AND VESICOURETERAL REFLUX HAD HAD UNDOCUMENTED URINARY TRACT INFECTIONS IN THE PAST.
ASYMPTOMATIC URINARY INFECTIONS ARE MORE COMMON IN GIRLS AT WHAT AGE.

WHAT ARE THE LIMITATIONS OF RETROSPECTIVE STUDIES MENTIONED IN THE REVIEW.
SELECCIONE UNA:

CASO CLÍNICO SERIADO 1/5

FEBRILE URINARY TRACT INFECTIONS IN CHILDREN
GIOVANNI MONTINI, N ENGL J MED 2011; 365:239-250
ACUTE PYELONEPHRITIS IS THE MOST COMMON SERIOUS BACTERIAL INFECTION IN CHILDHOOD; MANY AFFECTED CHILDREN, PARTICULARLY INFANTS, HAVE SEVERE SYMPTOMS. MOST CASES ARE READILY TREATED, PROVIDED DIAGNOSIS IS PROMPT, THOUGH IN SOME CHILDREN FEVER MAY TAKE SEVERAL DAYS TO ABATE. APPROXIMATELY 7 TO 8% OF GIRLS AND 2% OF BOYS HAVE A URINARY TRACT INFECTION DURING THE FIRST 8 YEARS OF LIFE. FEBRILE URINARY TRACT INFECTIONS HAVE THE HIGHEST INCIDENCE DURING THE FIRST YEAR OF LIFE IN BOTH SEXES, WHEREAS NONFEBRILE URINARY TRACT INFECTIONS OCCUR PREDOMINANTLY IN GIRLS OLDER THAN 3 YEARS. AFTER INFANCY, URINARY TRACT INFECTIONS CONFINED TO THE BLADDER ARE GENERALLY ACCOMPANIED BY LOCALIZED SYMPTOMS AND ARE EASILY TREATED. IN CONTRAST, THE PRESENCE OF FEVER INCREASES THE PROBABILITY OF KIDNEY INVOLVEMENT (SENSITIVITY, 53 TO 84%; SPECIFICITY, 44 TO 92%) AND IS ASSOCIATED WITH AN INCREASED LIKELIHOOD OF UNDERLYING NEPHROUROLOGIC ABNORMALITIES AND A GREATER RISK OF CONSEQUENT RENAL SCARRING. KIDNEY SCARRING RELATED TO URINARY TRACT INFECTIONS HAS BEEN CONSIDERED A CAUSE OF SUBSTANCIAL LON-TERM MORBIDITY. THUS, CHILDREN WITH PROVEN INFECTIONS HAVE BEEN INTENSIVELY EVALUATED AND TREATED, AND THEY HAVE OFTEN UNDERGONE SURGERY OR HAVE RECEIVED LONG-TERM ANTIBIOTIC PROPHYLAXIS. SUCH APPROACHES HAVE BEEN QUESTIONS. A NUMBER OF TRIALS HAVE BEEN CONDUCTED OR ARE UNDER WAY TO DETERMINE OPTIMAL APPROACHES TO THE ASSESSMENT AND MANAGEMENT OF INITIAL FEBRILE URINARY TRACT INFECTIONS AND SUBSEQUENT INTERVENTIONS FOR THEM.

LONG TERM CONSEQUENCES
APPROXIMATELY 60% OF CHILDREN WITH FEBRILE URINARY TRACT INFECTIONS, IF EVALUATED DURING OR JUST AFTER THE INFECTION, HAVE VISIBLE PHOTON DEFECTS ON RENAL SCINTIGRAPHIC STUDIES WITH TECHNETIUM-99M-LABELED DIMERCAPTOSUCCINIC ACID (DMSA)-FINDINGS CONSIDERED EVIDENCE OF PARENCHYMAL LOCALIZATION (PYELONEPHRITIS). OF THESE, 1 0 TO 40% WILL HAVE PERMANENT RENAL SCARRING, UNRELATED TO AGE. THE LONG-TERM MEDICAL RISK OF INFECTION-RELATED SCARRING IN PREVIOUSLY HEALTHY KIDNEYS ARE INCOMPLETELY UNDERSTOOD. FEW POPULATION-BASED, FOLLOW-UP STUDIES HAVE BEEN PERFORMED. A SWEDISH STUDY FOLLOWED 57 CHILDREN WITH NONOBSTRUCTIVE RENAL SCARRING AND 51 MATCHED SUBJECTS WITHOUT RENALSCARRING AT UROGRAPHIC EXAMINATION, 16 TO 26 YEARS AFTER  A FIRST SYMPTOMATIC URINARY TRACT INFECTION. CHILDREN WITH UNILATERAL SCARS AND THOSE WITHOUT SCARS HAD SIMILAR GLOMERULAR FILTRATION RATES AT THE END OF FOLLOW-UP; HOWEVER, THE MEDIAN GLOMERULAR FILTRATION RATE IN SEVEN CHILDREN WITH BILATERAL SCARS DECREASES FROM 94 ML PER MINUTE PEER 1.73 M2 OF BODY-SURFACE AREA TO 84 ML PER MINUTE PER 1.73M2. NO DIFFERENCE IN AMBULATORY 24-HOUR BLOOD PRESSURE WAS FOUND BETWEEN CHILDREN WITH SCARS AND THOSE WITHOUT SCARS. THE FEW PROSPECTIVE STUDIES THAT HAVE BEEN PERFORMED SHOWED A LOW RATE OF LONG-TERM CONSEQUENCES. IN THE INTERNATIONAL REFLUX STUDY IN CHILDREN HYPERTENSION WAS REPORTED IN 4 OF 252 PATIENTS (1.6%) WITH REFLUX, MAINLY GRADE IV, PROSPECTIVELY FOLLOWED FOR 10 YEARS. (THE CLASSIFICATION OF VESICOURETERAL REFLUX IS EXPLAINED IN). ONE OF THE 133 CHILDREN WHOSE GLOMERULAR FILTRATION RATE WAS MEASURED HAD A CLEARANCE THAT HAD FALLEN BELOW THE MINIMAL STUDY ENTRY LEVEL OF 70 ML PER MINUTE PER 1.73M2 .30 MOST OF THE PROSPECTIVE STUDIES ARE LIMITED BY RELATIVELY SHORT FOLLOW-UP. IN CONTRAST, RETROSPECTIVE STUDIES HAVE SUGGESTED THAT RENAL SCARRING RELATED TO URINARY TRACT INFECTION CARRIES A CLINICALLY SIGNIFICANT RISK, WITH HIGH SUBSEQUENT RATES OF CHRONIC KIDNEY DISEASE (UP TO 20%), HYPERTENSION (20% TO 40%), AND PREECLAMPSIA (10 TO 20%). SUCH RETROSPECTIVE STUDIES ARE LIMITED BY REFERRAL BIAS IN THAT SPECIALIZED CENTERS MAY NOT SEE THE VAST MAJORITY OF CHILDREN, WHO HAVE UNCOMPLICATED FEBRILE URINARY TRACT INFECTIONS. IN ADDITION, SOME RETROSPECTIVE STUDIES RECRUITED PATIENTS BEFORE THE WIDESPREAD AVAILABILITY OF PRENATAL ULTRASONOGRAPHIC SCREENING. FURTHERMORE, OTHER STUDIES ASSUMED THAT ALL PATIENT WITH CHRONIC KIDNEY DISEASE AND VESICOURETERAL REFLUX HAD HAD UNDOCUMENTED URINARY TRACT INFECTIONS IN THE PAST.
ASYMPTOMATIC URINARY INFECTIONS ARE MORE COMMON IN GIRLS AT WHAT AGE.

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A 69 YEAR-OLD LADY PRESENTS TO YOU COMPLAINING OF BEING NON-SPECIFICALLY UNWELL OVER THE LAST MONTH. SHE IS STIFF ESPECIALLY IN THE MORNINGS AND HAS DIFFICULTY LIFTING HER HANDS TO COMB HER HAIR. HER ARMS AND SHOULDERS ACHE CONSTANTLY AND SHE HAS JAW PAIN WHEN CHEWING. SHE HAS LOST 4KG IN WEIGHT AND HAS A PERSISTENT HEADACHE. SHE SMOKES 10 CIGARETTES A DAY AND CONSUMES 10 UNITS OF ALCOHOL A WEEK. APART FROM TENDERNESS WITH REDUCED MOBILITY IN THE PROXIMAL MUSCLES OF HER ARMS AND LEGS, EXAMINATION IS NORMAL. INVESTIGATIONS: HB 9.9 G/DL (11.5- 16.5) WCC 13.9 X109/L (4-11 X109) PLATELETS 400 X 109/L (150-400 X109) .

PLASMA SODIUM 139 MMOL/L (137-144)
PLASMA POTASSIUM 4.7 MMOL/L (3.5-4.9) PLASMA UREA 5.0 MMOL/L (2.5-7.5) PLASMA CREATININE 109 ΜMOL/L (60-110)
PLASMA GLUCOSE 5.9 MMOL/L (3.0-6.0) BILIRUBIN 15 UMOL/L (1-22) PLASMA ALKALINE PHOSPHATASE 390 U/L (45-105)
PLASMA ASPARTATE TRANSAMINASE 65 U/L (1-31) PLASMA CREATINE KINASE 150 U/L (24-170) WHAT IS THE MOST LIKELY DIAGNOSIS?
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A 30 YEAR-OLD MALE COMPANY DIRECTOR IS REFERRED TO YOU FROM CASUALTY WITH A 24 HOUR HISTORY OF A PAINFUL AND SWOLLEN LEFT KNEE. HE DENIES ANY HISTORY OF TRAUMA AND DOES NOT HAVE ANY PREVIOUS HISTORY OF JOINT PROBLEMS. OVER THE LAST TWO DAYS, HE HAS ALSO NOTICED REDNESS AND SORENESS IN BOTH EYES. HE IS MARRIED, A NON-SMOKER AND CONSUMES ABOUT 10 UNITS OF ALCOHOL WEEKLY. HE HAS RETURNED FROM A BUSINESS TRIP TO AMSTERDAM A FORTNIGHT AGO. ON EXAMINATION, HIS TEMPERATURE IS 38.50C. HIS EYES ARE RED AND HE HAS A BROWN MACULAR RASH ON THE SOLES OF HIS FEET. HIS LEFT KNEE IS HOT, SWOLLEN AND TENDER TO PALPATE. NO OTHER JOINT APPEARS TO BE AFFECTED. INVESTIGATIONS: HB 12.9 G/DL (13.0-18.0) WBC 14.0 X109/L (4-11 X109 PLATELETS 200 X109/L (150-400 X109) ESR 75 MM/HR (0-15). PLASMA SODIUM 140 MMOL/L (137-144) PLASMA POTASSIUM 4.1 MMOL/L (3.5-4.9) PLASMA UREA 5.6 MMOL/L (2.5-7.5)
PLASMA CREATININE 100 ΜMOL/L (60-110) BLOOD CULTURES NO GROWTH AFTER 48 HOURS URINALYSIS NO BLOOD, GLUCOSE OR PROTEIN DETECTED KNEE X-RAY SOFT TISSUE SWELLING AROUND LEFT KNEE WHAT IS THE MOST LIKELY DIAGNOSIS?
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A 17-YEAR-OLD MAN WAS BEING INVESTIGATED FOR A LONG HISTORY OF MALAISE. HIS PAST MEDICAL HISTORY INCLUDED RECURRENT EPISODES OF ANAEMIA BUT THE CAUSE HAD NEVER BEEN ESTABLISHED. THERE WAS NO PAST HISTORY OR FAMILY HISTORY OF NOTE AND APART FROM THE MALAISE HE REPORTED NO OTHER SYMPTOMS. ON EXAMINATION HE WAS MILDLY JAUNDICED. HE HAD A BLOOD PRESSURE OF 120/75 MMHG AND HIS PULSE WAS 80 BEATS PER MINUTE. HIS SPLEEN WAS PALPABLE 6CM BELOW THE LEFT COSTAL MARGIN. NO OTHER ABNORMALITY IS FOUND. RESULTS OF INVESTIGATIONS ARE SHOWN BELOW: HAEMOGLOBIN 8.4 G/DL (13.0-18.0) MCV 76 FL (80-96) MCH 29 PG (28-32) MCHC 40 G/DL (32-35) WHITE CELL COUNT 11.0 X109/L (4-11 X109) NEUTROPHILS 7.0 X109/L (1.5-7 X109) LYMPHOCYTES 3.2 X109/L (1.5-4 X109) MONOCYTES 0.5 X109/L (0-0.8 X109) EOSINOPHILS 0.2 X109/L (0.04-0.4 X109) BASOPHILS 0.1 X109/L (0-0.1 X109)PLATELETS 366 X109/L (150-400 X 109) RETICULOCYTE COUNT 9.0% SERUM FERRITIN 45 G/L (15-300) SERUM FOLATE 1.2 G/L (2.0-11.0) DIRECT COOMBS TEST NEGATIVE OSMOTIC FRAGILITY TEST: INCREASED OSMOTIC FRAGILITY SERUM SODIUM 139 MMOL/L (137-144) SERUM POTASSIUM 4.5 MMOL/L (3.5-4.9) SERUM UREA 4.5 MMOL/L (2.5-7.5) SERUM CREATININE 60 ΜMOL/L (60-110) SERUM ASPARTATE AMINOTRANSFERASE 30 U/L (1-31) SERUM ALKALINE PHOSPHATASE 56 U/L (45-105) SERUM TOTAL BILIRUBIN 102 ΜMOL/L (1-22) SERUM PHOSPHATE 0.9 MMOL/L(0.8-1.4) SERUM CORRECTED CALCIUM 2.2 MMOL/L (2.2-2.6) SERUM ALBUMIN 40 G/L (37-49) SERUM TOTAL PROTEIN 65 G/L (61-76) THE BLOOD FILM SHOWED RED CELL POIKILOCYTES WITH SPHEROCYTES AND SOME POLYCHROMASIA. WHAT IS THE DIAGNOSIS?
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