 Infection of the flexor tendon sheaths of the hand, represents a potential surgical emergency, due to these being closed compartments and swelling can result in necrosis. The same does not tend to occur in extensor tendons as they are open compartments.
Infections to the flexor tendon sheath usually occur following a penetrating injury to the hand. The infection course can be surprisingly rapid and aggressive. Beware the immunocompromised patient, as they can have a much more rapid deterioration. The infection can result, in its mildness form, in some tightness and restriction of movement in the tendon involved. In its most serious form, it can cause tendon necrosis, loss of limb, or even mortality. In most cases the decision for surgical intervention and washout is a clinical one. Inflammatory markers such as white cell count and C-reactive protein do not help if they are normal, as their negative predictive value is approximately 4% and 13% respectively(1). Kanavel's sign(2) is a clinical sign made up of four parts. It assists in predicting pyogenic flexor tenosynovitis of the hand, however has never been validated. Also the absence of one or more of it’s parts does not exclude the condition. In fact all four parts have been found to occur in only about 50% of cases(3) The sign consists of four parts: 1 Flexed posture of the finger: The finger is held in slight flexion for comfort. 2 Circumferential swelling of the finger. 3 Percussion Tenderness along the whole length of the Flexor sheath . 4 Severe Pain if attempt to extend the affected finger. Tenderness along the length of the tendon sheath tends to be a late sign, but an important one. Perhaps the most frequent sign is the circumferential swelling of the finger(4), but the most helpful may be severe pain on finger passive extension(5). The signs may also be less prominent in the thumb and fifth finger as these become the radial and ulnar bursa respectively, providing decompression. The most common organisms involved include: 1 Staphylococcus aureus 2 MRSA 3 Pseudomonas aeruginosa 4 Streptococcus species However rarer organisms such as Pasteurella, Listeria. Neisseria gonorrhoea and Clostridium. The bottom line, is be careful not to send these patients home. An infected swollen finger that is painful to move, needs to be assessed by the hand surgeons in your hospital. References: 1 Bishop GB, Born T, Kakar S, Jawa A. The diagnostic accuracy of inflammatory blood markers for purulent flexor tenosynovitis. J Hand Surg Am 2013;38:2208-2211 2 Kanavel AB. The symptoms, signs, and diagnosis of tenosynovitis and fascial-space abscesses. In Infections of the Hand. 1st ed. Philadelphia, PA: Lea & Febiger; 1912:201–226. 3 Dailiana ZH, Rigopoulos N, Varitimidis S, Hantes M, Bargiotas K, Malizos KN. Purulent flexor tenosynovitis: factors influencing the functional outcome. J Hand Surg Eur. 2008;33:280–285. 4 Pang HN, Teoh LC, Yam AK, Lee JY, Puhaindran ME, Tan AB. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2007;89:1742–1748. 5 Neviaser RJ, Gunther SF. Tenosynovial infections in the hand: diagnosis and management. Instr Course Lect. 1980;29:108–128
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CEREBRAL OEDEMA IN DKA: DO WE REALLY KNOW THE CAUSE?
We recently had a child with DKA in our department and the subject of fluid resuscitation came up. Also the Queensland Government guidelines on the Emergency Management of children with DKA has recently been produced. I thought it was timely to revisit a blog I wrote in 2014 on the evidence on this topic, as well as set up a teaching module on DKA ( more on this at the end) Cerebral oedema is the most feared complication in children presenting with Diabetic Ketoacidosis (DKA). It occurs in about 1% of cases but has a mortality rate of up to 90% (Waldorf J et al Diabetes Care 2006; 29:1150-9). Patients will have a decreased conscious state and may also have cranial nerve palsies, headache and/or bradycardia and hypertension. Its incidence has remained the same since it was described in 1936 and although we have clues as to what may contribute to it, and we know that some patients have subclinical cerebral oedema even at presentation(Krane et al NEJM 1985;312:1147-51), we still can't predict who will get it, nor greatly affect its high rate of mortality. There are theories of causative factors, most of which are vasogenic or osmotically based, but the studies are small or retrospective, or both. WHAT CAUSES IT? - THEORETICALLY One theory relates to osmolytes accumulating in brain cells. These are the compounds that maintain normal cell volumes. As extracellular osmolality decreases rapidly with treatment, water flows rapidly onto these cells causing the brain to swell. Another theory relates to Na+ / H+ exchanger, such that a correction of acidosis results in Na and water passing onto the brain cells, resulting in oedema. WHAT CAUSES IT? - IN PRACTICAL TERMS We believe that the following increase the chance of developing cerebral oedema: 1 Newly diagnosed diabetes 2 Duration of symptoms 3 Rapid change in Osmolality (2xNa + U + Glc): i.e., a rapid decrease in Glucose and a decrease in Sodium 4 Initial pH < 7.1 ................ and in more recent studies (Glaser N et al NEJM 2001;344:264-269) 5 Decrease in CO2 6 Increased Urea 7 If treated with Bicarbonate WHAT DOES THIS MEAN IN TERMS OF TREATMENT? FLUIDS: If the patient is hypotensive and crashing then fluid resuscitation is necessary. No question about it. However, how much we give may matter. In some of the work published there is an indication that more than 40ml/kg given over the first 4 hours may predispose to cerebral oedema. We seem to be conditioned to give 20ml/kg to every child. My approach is a little less aggressive. I aim at 5ml/kg if the child is very unwell and crashing. I then review and give it a little time ( that may only be minutes) before more fluids are given. The point is, unless the child is crashing we don't have to give large volumes, we can pull back a little. The recommendations look at tolerating a systolic blood pressure of (70 + 2 x age)mmHg. We must remember that kids don’t have much room, when they decompensate and that hypotension is a late sign. However it is this very group of children that we may be harming. If the blood pressure is OK, leave them be. If you really have to give fluids ( because it is so conditioned that its an automatic reflex), give 1ml/kg and wait. The usual approach to fluids is to calculate the deficit and ongoing maintenance needs and give over 48 hours. INSULIN AND GLUCOSE LEVELS: Large rapid drops in glucose, or a rapid decrease in osmolality can, according to the osmotic theory, cause cerebral oedema. Hoorn et al (J pediatr 2007:150: 467-473), found that a drop in osmolality from 304 + 5 to 290 + 5, was associated with increased cerebral oedema. WHAT SHOULD WE TAKE AWAY FROM ALL OF THIS AND WHAT SHOULD WE DO? The evidence isn't great. What we see is that the more acidotic you are, the more deranged your electrolytes, the more abnormal your physiology, the worst you do. The sicker kids did badly. Common sense. Firstly it's important to say that it's very rare that you will see one of these cases unless you are working in an ED that sees lots of kids. That's why its even more important to know what to do, because its not that frequent. If a child is sick and haemodynamically crashing, then give fluids. I don't give 20ml/kg of normal saline right away. I will give 5-10ml/kg and then review. I can always give more if needed. I don't give a bolus of insulin, I start an infusion(after fluids are initiated and probably not before 1-2 hours) and wait for gentle lowering of the blood sugar i.e.., < 5mmol/L drop per hour. Things improve over hours. Nothing needs to happen quickly here. If I think a child has cerebral oedema, mannitol 1g/kg IV is the treatment of choice. You must discuss these patients with endocrine/Paediatrics and ICU. If the conscious state deteriorates to the point where protection of the airway is needed, or if airway control is necessary to paralyse and lower intracranial pressure( if this indeed assists in this case), then beware not to hyperventilate the patient. Hypocapnia from mechanical ventilation has been associated with this condition(Glaser N et al NENM 2001;344:264-269) Cerebral oedema, if it occurs, is a difficult condition to treat and the outcomes aren't good. We don't really know if our treatment contributes to the development. However, we need to do everything we can, to ensure it doesn't. Click below to complete a real time case module online, that will help reinforce the management of DKA.
The ambulance bring a patient in on a rebreather. She is elderly and has been unwell for the last few days. Her respiratory rate is 32, heart rate is 125 and sats are 90%. She is afebrile and examination is normal apart for a few creeps in both bases. A set of gases reveals the following: pH 7.3 PaO2 63 PaCO2 37 HCO3 20 SaO2 90% Does she meet Criteria for Non-Invasive Ventilation(NIV)? Yes she does? What type of NIV would you use; CPAP or BiPAP? What type of NIV would you use for: (A) Acute Pulmonary Oedema? (b) COPD? (c) Asthma? .... and why ... all answers in the 9 minute video below: You place the patient on BiPAP (settings EPAP 6 / IPAP 11) and wean down to 50% and the patients gases improve markedly: paO2 137 paCO2 39 The patients respiratory rate is still high at 28 breaths per minute. What setting would you change on the machine to assist the patient?
I think it’s relative lack of uptake is related to the fact that we do it intuitively. If your patient has a heart rate that equals their systolic blood pressure, you’d worry wouldn’t you? Most physicians would look at a sagging blood pressure and decide to treat that patient.
Rady(1) found it a useful measure of cardiovascular performance and a marker for predicting the onset of hypotension; an index of >0.8, being associated with a 95% sensitivity for predicting shock. It has been shown to predict which emergency patients need vasopressors within 72 hours (2), as well as who may suffer organ failure. Montoya et al (3) found that in trauma patients a SI >0.9 resulted in increased mortality at 24 hours. It has also been used to identify severely injured children (4). However in children, a complicating factor, is that it requires age adjustment, due to the fact that children’s heart rates and blood pressures vary with age. Perhaps the one area where I know of it being used most, is in predicting post intubation hypotension (5,6). It certainly does this well when the SI is greater than 0.8-0.9. A high shock index is used to treat the patient’s blood pressure before any induction is given. The aim in some centres is a SI = 1. You know that when you’re about to intubate, if your patients blood pressure is low you’ll probably have hypotension post intubation. Certainly start by filling the tank. Give a fluid bolus of 250-500mL of Normal Saline and as I do, leave the line open(unless there are contraindications) whilst intubation is undertaken. In Australia we would give Metaraminol, to raise the BP. It comes either in 10mg vials or is premixed to 0.5mg/mL. The dose is 0.25-1mg IV and titrate. Induction drugs need to be rethought and instead of using Propofol, would prefer Ketamine and Rocuronium. So there it is; the SHOCK INDEX. A lot of studies on it, but not sure how much it is used. It may very well have a place in allowing us to identify that patient that is progressively worsening, with smaller changes in their vitals and it certainly has a role in intubation. References:
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AuthorDr Peter Kas Archives
November 2016
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